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The suitability of blood collected on filter papers in comparison with corresponding conventional serum samples in the diagnosis of bovine anaplasmosis was studied using the Complement Fixation Test (CFT), DOT-ELISA, Western immunoblot and Rapid Card Agglutination Test (RCAT). Dried blood on Whatman filter paper no. 1 was eluted in 1.8 ml of PBS 0.05% Tween 20 given an initial dilution of 1:100. The reactivity in both DOT-ELISA and Western immunoblotting was similar to that obtained with the sera diluted 1:100. Filter paper samples gave lower reactivity in all the tests as compared with corresponding serum samples. There was no significant difference in the reactivity between the eluates from filter papers stored at room temperature and those stored at 4°C. Storage at room temperature did not significantly affect reactivity for up to 6 months. Eluates from filter papers stored for 6 months at room temperature continued to give similar reactivity to those from freshly prepared filter papers in both DOT-ELISA and Western blot, and in the Rapid Card Agglutination Test. It is concluded that collecting blood on filter papers is a suitable technique for large-scale screening and for seroepidemiological studies on anaplasmosis, and offers many advantages especially in developing countries where transport and cold chain facilities are a major constraint. [ABSTRACT FROM AUTHOR]

Major studies are still lacking on the impact of differing intensities of long-term donor plasmapheresis, not only on total serum protein, albumin and immunoglobulin G (IgG), but also on humoral and cellular immunity, red cell and iron metabolism, and biochemical cardiovascular risk markers. Three groups of donors, comprising 483 individuals undergoing differing intensities of long-term serial plasmapheresis, were entered into a cross-sectional study. A fourth control group consisted of 100 non-donors. In addition to measuring total protein, albumin and IgG levels, we determined parameters of humoral and cellular immunity, red cell and iron metabolism and recognized biochemical cardiovascular risk factors. The median annual net amount of plasma donated by the three donor groups was 37, 16 and 10 l, respectively ( P < 0·0001). Donors had significantly lower total serum protein, albumin and IgG levels than non-donors ( P < 0·0001), but the intensity of plasmapheresis had no influence on those parameters. Like non-donors, all plasma donors had normal humoral and cellular immunity. No increased rates of iron store depletion were observed in the three groups of plasma donors. Plasma donors were not at increased cardiovascular risk. Regular donor plasmapheresis of up to 45 l of plasma per year appears to be as safe as more moderate plasmapheresis programmes, with respect to the parameters analysed in this study. Individuals donating under these conditions did not develop impaired humoral and cellular immunity, iron store depletion, or increased cardiovascular risk with regard to established biochemical risk markers. Prospective studies are required to determine more exactly than in retrospective analyses the reasons why donors withdraw from plasmapheresis programmes. [ABSTRACT FROM AUTHOR]

The 48 G>C transversion in exon 1 of the RHCE gene leads to Trp16Cys, usually present in the conventional RHCE Ce, while Trp16 is associated with RHCE ce. The presence of Cys16 in RHCE ce is associated with the R0 (Dce) haplotype in Africans, leading to a weak ‘e’ antigen expression on red blood cells (RBCs). VS is a common red cell antigen in individuals of African descent and results from a single point mutation in exon 5 of the RHCE (733C>G), leading to Leu245Val substitution; VS positivity is also associated with weak expression of ‘e’. This study investigated the association of Cys16 and/or VS with the RHCE ce alleles in a cohort of sickle cell disease (SCD) patients phenotyped as R0r or R0R0 and rr. DNA samples from 58 SCD patients were tested for the 48 G>C transversion, encoding Cys16, by allele-specific polymerase chain reaction (PCR). We also amplified exon 5 of the RHCE by PCR and subjected the amplified product to restriction fragment length polymorphism analysis, using BfaI, in order to determine the VS status. Further cDNA analysis was performed on three samples to verify whether the mutations were located on the same or on different alleles. Fifty-six of the 58 SCD patients studied (97%) were heterozygous for 48G/48C (Cys16). Of these, 18 (32%) were also heterozygous for 733C/G (245Val). All of these 18 samples showed weak ‘e’ expression on RBCs when tested with at least one monoclonal antibody to e antigen. cDNA sequencing of three of 18 patient samples showed that the genes encoding Cys16 and Val245 (VS) were on different alleles. We found a high incidence of Cys16 associated with the RHCE ce in our SCD cohort. A high percentage of these patients were also found to be heterozygous for VS. cDNA analysis showed that, in at least three samples, the two mutations were on different alleles, with consequent weakening of expression of the e antigen on RBCs. [ABSTRACT FROM AUTHOR]

Background: Lewis serologic reagents frequently give inaccurate phenotyping results. Furthermore these serologic reagents are often used in nonserologic assays such as inhibition and immunohistochemistry. In both scenarios knowledge of the fine specificity and cross-reactivity of these reagents will improve the quality of results obtained.Study Design and Methods: A range of contemporary and historical workshop and developmental Lewis reagents including mouse monoclonal (MoAb) and human and goat polyclonal (PoAb) reagents were evaluated. All were evaluated both against Lewis kodecytes expressing only single Le(a) , Le(b) , ALe(b) , BLe(b) , Le(x) , Le(y) , ALe(y) , or BLe(y) antigens and against the same antigens inkjet printed on a paper-based microplate and analyzed by enzyme immunoassay. Nine clinical samples were also evaluated. A kodecyte antigen dilution sensitivity assay was used to establish the ratio of Le(b) antigen between group A1 /A2 and O RBCs.Results: A continuum of cross-reactivity from Le(x) through to H was observed with MoAbs. All PoAb and few MoAb anti-Le(a) samples and reagents cross-reacted to some degree with Le(b) antigen. Some PoAb and MoAb anti-Le(b) did not cross-react with Le(a) . All polyclonal goat anti-Le(b) reagents showed substantial activity against ALe(b) and BLe(b) , while no MoAb reagent had this activity. A1 RBCs had less than half the Le(b) antigen of A2 /O RBCs.Conclusions: Substantial cross-reactivity of both MoAbs and PoAbs with related antigens highlights the risks of using serologic reagents in nonserologic assays or against synthetic antigens. The lack of ALe(b) activity in anti-Le(b) MoAbs explains their poor performance against blood group A1 Le(a-b+) phenotypes. [ABSTRACT FROM AUTHOR]

In binocular stereo matching, there has been a problem of low matching accuracy and noise immunity in discontinuous regions and weak‐textured regions. This paper proposes a stereo matching algorithm based on an improved adaptive support window. In the cost computation stage, first, according to the preset arm length and colour threshold, a cross‐based arm is obtained, which centres on the pixel to be matched; then the adaptive regions of the vertical arm and the horizontal arm are constructed respectively, which have different shape and size. Finally, the union of the two adaptive regions is used as the final support window of Census transform. Performance evaluations on Middlebury stereo data sets demonstrate that the proposed algorithm outperforms other seven most challenging stereo matching algorithms. The mismatching rate of this algorithm is greatly reduced, and the anti‐noise performance is also improved considerably. Because the construction of the adaptive region is based on strict criteria and comprehensive consideration, the algorithm proposed in the paper can improve the matching accuracy in the weak‐textured regions and discontinuous disparity regions. [ABSTRACT FROM AUTHOR]

Lists forthcoming research papers on immunology published in the journal "Immunology."

Presents several developments in the veterinary medicine. Identification of keel and furculum damage in laying hens; Detection of antigens in fresh and autolysed tissue; Hypervaccination with marker vaccines against bovine herpesvirus type 1.

Vitiligo is caused by an autoimmune reaction against melanocytes leading to melanocyte loss. The cause of vitiligo is an interaction between genetic susceptibility and environmental factors. Both the adaptive immune system—through cytotoxic CD8+ T cells and melanocyte specific antibodies—and the innate immune system are involved in these immune processes in vitiligo. While recent data stressed the importance of innate immunity in vitiligo, the question remains why vitiligo patients' immune response becomes overly activated. Could a long‐term increase in innate memory function, described as trained immunity after vaccination and in other inflammatory diseases, play a role as an enhancer and continuous trigger in the pathogenesis of vitiligo? After exposure to certain stimuli, innate immune system is able to show an enhanced immunological response to a secondary trigger, indicating a memory function of the innate immune system, a concept termed trained immunity. Trained immunity is regulated by epigenetic reprogramming, including histone chemical modifications and changes in chromatin accessibility that cause sustained changes in the transcription of specific genes. In responses to an infection, trained immunity is beneficial. However, there are indications of a pathogenic role of trained immunity in inflammatory and autoimmune diseases, with monocytes presenting features of a trained phenotype, resulting in increased cytokine production, altered cell metabolism through mTOR signaling, and epigenetic modifications. This hypothesis paper focusses on vitiligo studies that have shown these indications, suggesting the involvement of trained immunity in vitiligo. Future studies focusing on metabolic and epigenetic changes in innate immune cell populations in vitiligo could help in elucidating the potential role of trained immunity in vitiligo pathogenesis. [ABSTRACT FROM AUTHOR]

Aim: The aim of this observational study was to determine the immune status and function in young adults with cerebral palsy (CP) in comparison to typically developing individuals. Method: Blood samples from 12 individuals with CP (five males, seven females; mean age: 25 years 1 month (5 years 9 months); age range: 19–38 years) and 17 typically developing individuals (eight males, nine females; mean age: 31 years 4 months (6 years 2 months); age range: 20–40 years) were collected before, immediately after, and 1 hour after 45 minutes of frame running or running respectively. Independent t‐tests were used to compare heart rate, level of exertion, and baseline cell proportions between groups. Mixed model analysis of variance was utilized to investigate immune cell responses to exercise across groups. Results: Baseline levels of gamma delta (TCRγδ+) T‐cells were significantly higher (absolute percentage: +2.65, p = 0.028) in the individuals with CP. Several cell populations showed similar significant changes after exercise in both CP and typically developing groups. Cytotoxic (CD8+) T‐cells were only significantly elevated immediately after exercise in the typically developing participants (p < 0.01). Individuals with CP exhibited significantly lower heart rates (−11.1%, p < 0.01), despite similar ratings of perceived exertion. Interpretation: Elevated baseline TCRγδ+ T‐cells may indicate low‐grade inflammation in adults with CP. Although most of the cell populations showed typical responses to endurance exercise, the absence of response in CD8+ T‐cells in individuals with CP may indicate the need for higher intensity during exercise. What this paper adds: TCRγδ+ T‐cell baseline levels are elevated in adults with cerebral palsy (CP).The CD8+ T‐cell response to exercise was blunted in adults with CP.Exercise intensity is decisive for CD8+ T‐cell responses in individuals with CP. [ABSTRACT FROM AUTHOR]

Evidence of cognition in aneural cells is well‐establish in the literature. This paper extends the exploration of the mechanisms of cognition by considering whether or not aneural cells may be capable of irrational cognition, making associations based on coincidental similarities and circumstantial factors. If aneural cells do harness such semiosic qualities, as with higher‐level creativity, this might be how they are able to overcome old algorithms and invent tools for new situations. I will look at three examples of irrational learning in aneural systems in terms of semiotics: (1) generalisation in the immune system, based on viral molecular mimicry, whereby immune cells attack the self, which seems to be an overgeneralisation of an icon sign based on mere similarity, not identity, (2) the classical conditioning of pea plants to trope toward wind as a sign of light, which seems to be an association of an index sign based on mere temporal proximity, and (3) a pharmaceutical intervention to prevent pregnancy, using a conjugate to encrypt self with non‐self, which seems to be an example of symbol use. We identify irrational cognition easily when it leads to 'wrong' outcomes, but, if it occurs, it may also lead to favourable outcomes and 'creative' solutions. [ABSTRACT FROM AUTHOR]

Irritable bowel syndrome (IBS), one of the most prevalent functional gastrointestinal disorders, is characterized by recurrent abdominal pain and abnormal defecation habits, resulting in a severe healthcare burden worldwide. The pathophysiological mechanisms of IBS are multi‐factorially involved, including food antigens, visceral hypersensitivity reactions, and the brain–gut axis. Numerous studies have found that gut microbiota and intestinal mucosal immunity play an important role in the development of IBS in crosstalk with multiple mechanisms. Therefore, based on existing evidence, this paper elaborates that the damage and activation of intestinal mucosal immunity and the disturbance of gut microbiota are closely related to the progression of IBS. Combined with the application prospect, it also provides references for further in‐depth exploration and clinical practice. [ABSTRACT FROM AUTHOR]

There is growing scientific interest in immunity mandates/passports (IMP) for viral diseases in light of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. IMP isolate those who remain nonimmune from various settings to reduce nonhousehold transmissions from the nonimmune and reduce severe/critical illness among the nonimmune. A major limitation in the scientific literature is that there are currently no methods to quantify how many nonimmune individuals need to be isolated to achieve these purported benefits. This paper develops a procedure for estimating the benefits of IMP using a novel variant of the number needed to treat which we call the number needed to isolate (NNI). We use data from the SARS‐CoV‐2 pandemic to demonstrate the properties and utility of the NNI and to inform the debate about IMP. We focus on data from the European Union, United Kingdom, United States, Canada, Australia, and Israel during the fall 2021 when the Delta (B.1.617.2) variant predominated. [ABSTRACT FROM AUTHOR]

Background: Currently, patients with diabetic erectile dysfunction (DMED) were not satisfied with the effects of first-line phosphodiesterase type 5 inhibitors (PDE5Is). Hence, this paper was designed to mine hub biomarkers in DMED and explore its potential mechanisms. Methods: Gene expression matrix of DMED was downloaded from the gene expression omnibus (GEO; GSE2457) dataset. The top 20 genes were selected based on the connectivity degrees in protein-protein interaction (PPI) network. Functional enrichment analysis was utilized to reveal DMED-related signaling pathways. We also explored the roles of immunity, m6A, ferroptosis, or cuproptosis in DMED and constructed Sprague Dawley (SD) rats DMED model to verify gene expressions by quantitative real-time polymerase chain reaction (qRT-PCR). Results: Based on the threshold, a total of 122 differently expressed genes (DEGs) were identified in DMED, including 39 up-regulated and 83 down-regulated genes. Functional enrichment analysis implied that these DEGs were significantly enriched in peroxisome proliferator-activated receptors, ferroptosis, hypoxia-inducible factor 1 signaling pathways, and so on. SD rats DMED model was also successfully established by us and validated by intracavernous pressure/mean arterial pressure, Masson's trichrome staining, and immunohistochemical analysis. We further verified the expression of these top 20 genes from the PPI network by qRT-PCR in the SD rats DMED model and finally identified Sparc, Lox, Srebf1, and Mmp3 as hub biomarkers (all p<0.05). As for immunity and cuproptosis, our analysis indicated thatDMEDhad nothing to do with them (all p > 0.05). Actually, DMED was markedly associated with m6A regulators and ferroptosis. Conclusions:We identified Sparc, Lox, Srebf1, and Mmp3 as potential hub biomarkers in the SD rats DMED model for future drug development and found its significant associations with m6A regulators and ferroptosis, but not with immunity or cuproptosis. [ABSTRACT FROM AUTHOR]

Depression is a serious public health problem, and adolescence is an 'age of risk' for the onset of Major Depressive Disorder. Recently, we and others have proposed neuroimmune network models that highlight bidirectional communication between the brain and the immune system in both mental and physical health, including depression. These models draw on research indicating that the cellular actors (particularly monocytes) and signaling molecules (particularly cytokines) that orchestrate inflammation in the periphery can directly modulate the structure and function of the brain. In the brain, inflammatory activity heightens sensitivity to threats in the cortico‐amygdala circuit, lowers sensitivity to rewards in the cortico‐striatal circuit, and alters executive control and emotion regulation in the prefrontal cortex. When dysregulated, and particularly under conditions of chronic stress, inflammation can generate feelings of dysphoria, distress, and anhedonia. This is proposed to initiate unhealthy, self‐medicating behaviors (e.g. substance use, poor diet) to manage the dysphoria, which further heighten inflammation. Over time, dysregulation in these brain circuits and the inflammatory response may compound each other to form a positive feedback loop, whereby dysregulation in one organ system exacerbates the other. We and others suggest that this neuroimmune dysregulation is a dynamic joint vulnerability for depression, particularly during adolescence. We have three goals for the present paper. First, we extend neuroimmune network models of mental and physical health to generate a developmental framework of risk for the onset of depression during adolescence. Second, we examine how a neuroimmune network perspective can help explain the high rates of comorbidity between depression and other psychiatric disorders across development, and multimorbidity between depression and stress‐related medical illnesses. Finally, we consider how identifying neuroimmune pathways to depression can facilitate a 'next generation' of behavioral and biological interventions that target neuroimmune signaling to treat, and ideally prevent, depression in youth and adolescents. [ABSTRACT FROM AUTHOR]

Introduction: Already in its first implementation, the introduction of the Covid‐19 immunity certificate has generated some debate among the public. This debate might be a hindrance to the effective realization of this policy. This study aimed to systematically review published research evaluating public feeling of the Covid‐19 immunity certificate policy measure and to find which factors might influence its acceptance. Methods: We followed the scoping review methods manual by the Joanna Briggs Institute. We included studies with no time limits that presented novel data, and no exclusions have been made based on study design. We excluded articles that presented just expert opinions. Results: We found and reviewed 17 articles. The included studies were conducted in two main countries (the United Kingdom and Switzerland), with the rest from Israel, Italy, Spain, Germany, Australia, Taiwan and China. Both qualitative and quantitative studies were included, and nonrepresentative samples were mostly used to explore the public feeling about the Covid‐19 immunity certification. The included studies showed that public views on immunity certification are quite contradictory and influenced by age, gender, ethnicity, political orientation and attitudes towards Covid‐19 vaccination. The topic more often addressed by the included studies was the public's views on the positive and negative implications of the Covid‐19 immunity certificate in terms of ethical, legal and behavioural consequences of this measure. Conclusion: The varying acceptance rates are notable and may partly be linked to differences in demographics, Covid‐19 concerns and ideological beliefs, as seen in other health‐related tracking policies. Moreover, dominant factors behind the (un)success of this policy are complex and entangled with the cultural and political dimensions rather than being just technical. For this reason, it is important to expand psychosocial research to better understand the concerns behind health certifications and allow planning of culturally based and ethically sound suitable strategies. This would be very relevant to increasing public approval and compliance with this public health measure. Patient or Public Contribution: This does not apply to our work as it was a review paper. [ABSTRACT FROM AUTHOR]

In this paper, we formulate a generalized hepatitis B virus (HBV) infection model with two modes of infection transmission and adaptive immunity and investigate its dynamical properties. Both the virus‐to‐cell and cell‐to‐cell infection transmissions are modeled by general functions which satisfy some biologically motivated assumptions. Furthermore, the model incorporates three distributed time delays for the production of active infected hepatocytes, mature capsids, and virions. The well‐posedness of the proposed model is established by showing the non‐negativity and boundedness of solutions. Five equilibria of the model are identified in terms of five threshold parameters R0,R1,R2,R3$$ {R}_0,{R}_1,{R}_2,{R}_3 $$, and R4$$ {R}_4 $$. Further, the global stability analysis of each equilibrium under certain conditions is carried out by employing suitable Lyapunov function and LaSalle's invariance principle. Finally, we present an example with numerical simulations to illustrate the applicability of our study. Nonetheless, the results obtained in this study are valid for a wide class of HBV infection models. [ABSTRACT FROM AUTHOR]

Aeromonas hydrophila and A. veronii are widespread and important critical pathogenic bacteria in the aquaculture industry and cause severe economic damage. At present, magnolol has been proved to be a broad‐spectrum antibacterial activity, such as A. hydrophila, Staphylococcus aureus and Streptococcus mutans. In order to explore the cause of in vivo disease resistance of magnolol and promote its safe application in aquaculture, the pathological detection and changes in immune indicators of fish after feeding with magnolol were conducted in this paper. Results showed that the diets supplemented with magnolol (3 g magnolol/kg commercial feed) significantly increase the expression level of anti‐inflammatory cytokines (IL‐10, TGF‐β and IL‐4) in the liver of goldfish (p <.05). Additionally, the expression levels of proinflammatory cytokines (IL‐1β, IL‐8 and IFN‐γ) did not increase significantly. Subsequently, this study investigated the resistance of goldfish to A. hydrophila and A. veronii infection after feeding with magnolol. The results showed that the survival rates of treatment groups fed 3 g magnolol/kg commercial feed daily increased by 23.1% and 38.5% after 10 days post A. hydrophila and A. veronii (p =.0351) infection, respectively. Meanwhile, growth performance (body weight and length), major internal organs (liver, spleen, kidney and intestine) and the serum biochemistry indicators (ATL and AST) all exhibited no significant adverse effects after the goldfish fed with magnolol for 30 days. TP showed an increasing concentration in the treatment group (p <.05). Results of the mRNA expression of stress response indicated that the expression level of cyp1a and hsp70 was significantly down‐regulated after a 30‐day treatment (p <.05), and the two genes recovered to the similar level as the control group after a commercial feed diet. In brief, the diets supplemented with magnolol protected the host from the excessive immune response caused by A. hydrophila and A. veronii via enhancing its anti‐inflammatory capacity and had no adverse effects with feeding. [ABSTRACT FROM AUTHOR]

The fast and intermittent power changes in a direct‐current fast charging (DCFC) station impose adverse dynamic impacts on the station's host grid, particularly a weak AC distribution grid. This paper (i) investigates the impacts of the electric vehicle (EV) conventional DCFC station on its host distribution power system, and (ii) shows that the station can be enhanced by a battery energy storage system and an appropriate control strategy to mitigate the mutual dynamic interactions between the station and its host grid. The enhanced DCFC station is based on a variable‐voltage, common DC‐bus architecture which masks the station's internal dynamics, including rapid and intermittent EV charging processes, from the grid. Thus, it can be interfaced to a host grid, regardless of short‐circuit level, X/R ratio, and power capacity. The focus is also on the dynamic immunity of the DCFC facility to potential disturbances in its host weak‐grid. The reported studies are based on detailed time‐domain simulation of two DCFC stations in the PLECS software platform. [ABSTRACT FROM AUTHOR]

Global aquaculture development increased rapidly in recent years, and the sector has become one of the fastest‐growing industries in the animal‐derived food production system. However, disease outbreak remains a major challenge that hinders sustainable production through an advanced level of intensification. Recently, antibiotics applied have been restricted globally against aquatic disease outbreaks due to their apparent accumulation in the tissues, which imposes on the development of resistant bacteria. Naturally available medicinal plants were tested to combat some pathogens affecting humans and animals, as they contain a wide range of active substances that can induce biological functions. Currently, medicinal plants are being tested in aquaculture as a safe and eco‐friendly substance to modulate immune status, enhance growth performance and prevent fish disease. Moreover, different parts (e.g. leaf, flower and rhizome) and forms (e.g. crude, extract and active ingredient) of plants are used to modulate specific biological functions (e.g. growth promoter, anti‐stress, immunostimulants, appetite stimulation, antibacteria, anti‐parasite and anti‐virus). Medicinal plants are also used to defend the aquaculture animal from external stressors, such as poor water quality, high environmental temperature and overcrowding. This paper aims to provide information on the role of currently used medicinal plants on aquaculture animals and their action mechanisms. In conclusion, the current review suggested that the utilisation of medicinal plants remained untapped in uncovering the biological activities of active substances against a variety of diseases across diverse species of aquaculture animals. [ABSTRACT FROM AUTHOR]

Considering the effect of stochasticity including white noise and colored noise, this paper aims to study a hybrid stochastic cholera epidemic model with waning vaccine‐induced immunity and nonlinear telegraph perturbations. First, we derive a critical value ℛ0C related to the basic reproduction number ℛ0 of the deterministic model. The key aim of this paper is to generalize the θ‐stochastic criterion method proposed by the recent work (Han et al. in Chaos Solit Fract 140:110238, 2020) to eliminate nonlinear telegraph perturbations. Next, via constructing several θ‐stochastic Lyapunov functions and using the generalized method, we further prove that the stochastic model have a unique ergodic stationary distribution under ℛ0C>1. Results show that the prevention and control of cholera epidemic depend on low transmission rate and small telegraph perturbations. Finally, the corresponding numerical simulations are performed to illustrate our analytical results and a practical application on the Somalia cholera outbreak is shown at the end of this paper. [ABSTRACT FROM AUTHOR]

If there was any doubt of the primary role that plant secondary metabolites play in host–parasite co‐evolution, the "From the Cover" paper by Tan et al. (2019) featured in this issue of Molecular Ecology will lay these doubts to rest. The group's previous work on monarch butterflies (Danaus plexippus) infected with the protozoan pathogen Ophryocystis elektroscirrha (OE) demonstrated higher survival and lower spore load on high cardenolide‐producing milkweed (Asclepias curassavica) (Figure 1a) compared with low cardenolide‐producing milkweed (A. incarnata) (de Roode, Pedersen, Hunter, & Altizer, 2008) (Figure 1b). The mechanism of this protective effect is not directly clear, but a leading hypothesis is that the cardenolides confer protection through toxicity to the parasite. However, the role of the caterpillar immune system in managing this parasite is largely unknown. Novel insights into the influence of toxic plant metabolites on caterpillar immunity are explored in Tan et al. (2019). Using transcriptomics to probe this model system, the authors found that herbivore immune genes were down‐regulated and detoxification genes were up‐regulated when larvae were reared on the milkweed species with high cardenolide concentrations (A. curassavica). Surprisingly, immune genes were not significantly up‐ or down‐regulated in response to protozoan infection alone. This tantalizing result suggests that sequestered plant metabolites, not immunity, is reining in protozoan infections in these larvae, and promoting survival. As the authors point out, the strategy to invest in sequestration may come at a cost, which is to the detriment of the immune response (Smilanich, Dyer, Chambers, & Bowers, 2009). However, the cost becomes worth the investment when chemical sequestration takes on an antipathogen role. The novelty of the Tan et al. (2019) paper is that they show the investment in sequestration leading to a possible divestment in immunity. [ABSTRACT FROM AUTHOR]

The amino acid sequence of the light chain of a human monoclonal IgA1 (Mem) was established, in part by analogy with already known sequences. By homology its variable part was shown to belong to the VλI subgroup while the isotype-associated amino acid residues characterized it as Mcg+, Kern+ and Oz-. The normal primary structure of this chain was in contrast to its abnormal physical and antigenic properties: (a) its apparent molecular mass estimated by SDS/polyacrylamide gel electrophoresis, by gel filtration chromatography and by gradient ultracentrifugation was found to be lower by &assymp; 10% than the values (23.5 kDa) of ‘normal’ light chain used as controls; (b) the λI chain Mem, when tested in native state was not antigenically reactive. These abnormalities were reverted when the chain was treated with 8 M urea. These data suggest that the abnormal behaviour of λI chain Mere is at a conformational level. [ABSTRACT FROM AUTHOR]

Aim: The objective of this review is to describe the immunological mechanisms which facilitate maternal tolerance at the maternal‐placental interface, and to discuss how these mechanisms are disrupted in pre‐eclampsia. Methods: A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the immunological mechanisms which facilitate maternal tolerance in healthy pregnancy and pre‐eclampsia are presented in this article. Results: The maternal‐placental interface is the site where the immune tolerance begins and develops. Within the innate immunity, natural killer cells, macrophages and dendritic cells play a pivotal role in tolerance through regulation of inflammation. On the other hand, within the adaptive immunity, the correct increase of regulatory T cells is crucial for ensuring immune tolerance toward placental cells. Disturbances in maternal tolerance can lead to the appearance of pregnancy complications such as pre‐eclampsia, which has a considerable impact on perinatal morbidity and mortality. Conclusion: Our partial knowledge of immunological mechanisms involved in tolerance at the maternal‐placental interface indicates that pre‐eclampsia is characterized by alterations of this maternal immune tolerance, which could represent the origin of the disease. [ABSTRACT FROM AUTHOR]

Impaired regulation of immune function characterised by chronic inflammation together with a declining protective immune response is a major challenge to healthy ageing. It is therefore important to understand the mechanisms that regulate immune function and the impact of ageing upon such processes. Appropriate induction and resolution of the immune response require adequate availability of polyunsaturated fatty acids (PUFAs) for incorporation into cell membranes. However, humans are unable to synthesise PUFAs de novo and are dependent upon dietary intake for pre‐formed PUFAs or synthesis by the liver from the essential fatty acids, linoleic acid (LA, 18:2n‐6) and alpha‐linolenic acid (aLNA, 18:3n‐3). We have shown that activation of peripheral blood mononuclear cells increases PUFA biosynthesis from essential fatty acids via a mechanism that involves altered epigenetic regulation of a key gene in the pathway. Moreover, induction of PUFA synthesis is directly involved in the regulation of lymphocyte activation and proliferation. The aim of the Biotechnology and Biological Sciences Research Council responsive mode award described in this paper, 'How does polyunsaturated fatty acid biosynthesis regulate T‐lymphocyte function?', is to determine how PUFA biosynthesis regulates T‐cell function and the effect of ageing on this process. The project will identify points of regulation in the biosynthetic pathway and how these might influence the capacity for up‐regulation of PUFA synthesis in older individuals. We will use stable isotope tracers of LA and aLNA to determine whether newly synthesised PUFAs are preferential substrates for synthesis of lipid mediators and whether they are involved in formation of membrane microdomains that mediate cell signalling. [ABSTRACT FROM AUTHOR]

The immune function of living bodies has gained attention in engineering applications in a variety of fields. The authors proposed an immune network based on the immune response and researched its application to pattern recognition. The TH cell (helper T cell) that recognizes antigens in the immune response possesses diversity in order to fight various antigens and the function called interaction that communicates mutual information for correctly recognizing the antigens. The TH cell function successfully performs self-defense against unknown antigens. This paper proposes an immune network with the TH cell function added to an immune network we previously proposed. Specifically, we modeled the interaction and diversity functions of the TH cell in the matching process between input patterns and memory patterns. The proposed immune network is applied to a pattern recognition system of the alphabet and compared to a conventional method by numerical simulations. The proposed immune network exhibits lower incorrect recognition and rejections, and further improvement in the recognition rate over a conventional immune network by employing the process modeling the TH cell function. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 88(10): 12–22, 2005; Published online in Wiley InterScience (www.interscience. wiley.com). DOI 10.1002/ecjc.20162 [ABSTRACT FROM AUTHOR]

The Steering Committee for the Prevention and Control of Infectious Diseases in Asia recently conducted a survey of primary-care physicians in Asia, which revealed that many physicians administer boosters in their clinical practice and that there is considerable variation and uncertainty among physicians regarding this practice. This paper serves as a response to physicians’ uncertainties by reviewing the literature regarding the administration of hepatitis B vaccine boosters in high endemicity areas and presenting the Steering Committee's guidelines for booster administration. While there are few data to support a need for routine hepatitis B vaccine boosters as a public health measure, they help to provide reassurance of immunity against breakthrough infection in certain risk groups. In clinical practice, primary-care physicians must exercise their judgment regarding the need for booster vaccination on an individual basis. This paper examines the available literature on the administration and value of hepatitis B vaccine boosters, explores the differences between the public health approach and clinical practice, and provides guidelines for those who use boosters in high endemicity Asian populations. Relevant articles were identified through searches of MEDLINE (1975–2003) and the Cochrane Library, using‘hepatitis B’ and‘booster’ as primary search terms. Guidelines for those who decide to administer hepatitis B vaccine boosters include: boosting approximately 10–15 years after primary vaccination; boosting rather than not when monitoring of antibody levels is not feasible; boosting immunocompromised patients when the antibody to hepatitis B surface antigen titer falls below 10 mIU/mL; and boosting healthcare workers based on the endemicity of the particular country. [ABSTRACT FROM AUTHOR]

Toxoplasma gondii (T. gondii)‐associated polymorphic effector proteins are crucial in parasite development and regulating host anti‐T. gondii immune responses. However, the mechanism remains obscure. Here, it is shown that Toxoplasma effector dense granules 4 (GRA4) restricts host IFN‐I activation. Infection with Δgra4 mutant T. gondii strain induces stronger IFN‐I responses and poses a severe threat to host health. Mechanistically, GRA4 binds to phosphorylated TBK1 to promote TRIM27‐catalyzed K48‐ubiquitination at Lys251/Lys372 residues, which enhances its recognition by autophagy receptor p62, ultimately leading to TBK1 autophagic degradation. Furthermore, an avirulent Δgra4 strain (ME49Δompdc/gra4) is constructed for tumor immunotherapy due to its ability to enhance IFN‐I production. Earlier vaccination with ME49Δompdc/gra4 confers complete host resistance to the tumor compared with the classical ME49Δompdc treatment. Notably, ME49Δompdc/gra4 vaccination induces a specific CD64+MAR‐1+CD11b+ dendritic cell subset, thereby enhancing T cell anti‐tumor responses. Overall, these findings identify the negative role of T. gondii GRA4 in modulating host IFN‐I signaling and suggest that GRA4 can be a potential target for the development of T. gondii vaccines and tumor immunotherapy. [ABSTRACT FROM AUTHOR]

The disturbance of the inflammatory microenvironment is a frequent pathological trait of diabetic wounds, contributing to the emergence of numerous chronic illnesses. This is crucial in both the development and recovery of wounds caused by diabetes. This study aims to perform a bibliometric analysis of research on the inflammatory microenvironment within the domain of diabetic wounds (DW) over the past 10 years. The objective is to map out the current global research landscape, pinpoint the most significant areas of study and offer guidance for future research avenues. Our research involved querying the Web of Science Core Collection (WoSCC) database for all pertinent studies on the inflammatory microenvironment in diabetic wounds (DW). We utilized bibliometric tools such as CiteSpace, VOSviewer and R (version 4.3.1) to identify and highlight the most impactful studies in the field. The study encompassed a review of 1454 articles published from 2014 to 2023, highlighting China and the United States as pivotal nations in the research of the inflammatory microenvironment in diabetic wounds (DW). Within this sphere, the University of Michigan and Harvard University in the United States, along with Shanghai Jiaotong University in China, emerged as the most prolific institutions. WANG Y from China was identified as the most productive author, while KUNKEL SL from the United States received the most citations. The research primarily focuses on topics such as wound healing, repair processes, angiogenesis, oxidative stress and macrophage activity. Additionally, "macrophage" and "delivery" were pinpointed as the leading subjects with promising research potential in this area. Research on the inflammatory microenvironment of diabetic wounds is rapidly advancing through active international collaboration. The study of new mechanisms related to the inflammatory microenvironment and the development of novel materials for repair based on this microenvironment represent emerging fields of future research, particularly in terms of translational applications. This may offer guidance and novel perspectives for further research in the area of the diabetic wound inflammatory microenvironment. [ABSTRACT FROM AUTHOR]

The prevalence of bovine anaplasmosis was studied in 320 Zebu cattle randomly selected from three regions of Uganda (central, south-western and north-western) using DOT-ELISA, Western immunoblotting. Rapid Card Agglutination Test (RCAT), Capillary Tube Agglutination Test (CAT), Complement Fixation Test (CFT), and parasitological techniques. Dried blood on Whatman filter paper no. 1 was eluated in PBS 0.05% Tween 20 prior to testing at an initial dilution of 1.25. The incidence of parasitaemia ranged from 25% in the central region to 35% in the northwestern region and the serological prevalence was lower in the central region and highest in the north-west. Prevalence rates assayed by DOT-ELISA and Western immunoblotting were 1.5-fold greater than those tested with RCAT and 3-fold greater than in CAT. The overall prevalence rates by DOT-ELISA and Western immunoblotting compared favourably with CFT data. The present data utilizing dried blood on filter papers indicate that there is a high prevalence of anaplasmosis in those regions of Uganda surveyed and it confirms our observations and those of others that collecting blood on filter papers is a suitable technique for large-scale screening and for seroepidemiological studies. [ABSTRACT FROM AUTHOR]

Immunoglobulin (Ig) is the one of the main anti‐infective components of blood, colostrum and breast milk. It is the unique glycoprotein that defends the body from harmful bacteria, viruses and other environmental pathogens by either binding to them or by forming an encapsulating barrier. The expansion of antimicrobial and immunomodulatory products from natural sources for dietary supplementation in both animals and humans is an ever growing and thriving area of research. Purified Ig from sheep serum (ovine serum Ig) is one such candidate product. Recent work has shown the various biological effects of oral Ig in different animal models including its effect on growth, immunity, intestinal growth and gut barrier function. The objective of this paper is to review the results of recent studies demonstrating the effects of oral Ig in both pathogenic and non‐pathogenic animal models and to suggest a possible mechanism of its action. Overall, purified oral Ig improves growth of healthy (and challenged) rats and defends against enteric infection by immunomodulation, mucin protein and/or modification of commensal microbial composition. The findings contribute to knowledge of how orally administered ovine Ig can influence and enhance key indicators of gut function and overall growth performance in an animal model. [ABSTRACT FROM AUTHOR]

The prostate gland is a strictly androgen-dependent organ which is also the main target of infectious and inflammatory diseases in the male reproductive tract. Host defenses and immunity of the gland have unique features to maintain a constant balance between response and tolerance to diverse antigens. In this context, the effects of reproductive hormones on the male tract are thus complex and have just started to be defined. From the classical description of 'the prostatic antibacterial factor,' many host defense proteins with potent microbicidal and anti-tumoral activities have been described in the organ. Indeed, it has been proposed a central role for resident cells, that is, epithelial and smooth muscle cells, in the prostatic response against injuries. However, these cells also represent the target of the inflammatory damage, leading to the development of a Proliferative Inflammatory Atrophy-like process in the epithelium and a myofibroblastic-like reactive stroma. Available data on androgen regulation of inflammation led to a model of the complex control, in which the final effect will depend on the tissue microenvironment, the cause of inflammation, and the levels of androgens among other factors. In this paper, we review the current scientific literature about the inflammatory process in the gland, the modulation of host defense proteins, and the influence of testosterone on the resolution of prostatitis. [ABSTRACT FROM AUTHOR]

Sepsis is one of the major challenges in intensive care units, characterized by the complexity of the host immune status. To gain a deeper understanding of the pathogenesis of sepsis, it is crucial to study the phenotypic changes in immune cells and their underlying molecular mechanisms. We conducted Summary data‐based Mendelian randomization analysis by integrating genome‐wide association studies data for sepsis with expression quantitative trait locus data, revealing a significant decrease in the expression levels of 17 biomarkers in sepsis patients. Furthermore, based on single‐cell RNA sequencing data, we elucidated potential molecular mechanisms at single‐cell resolution and identified that LGALS9 inhibition in sepsis patients leads to the activation and differentiation of monocyte and T‐cell subtypes. These findings are expected to assist researchers in gaining a more in‐depth understanding of the immune dysregulation in sepsis. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) are emerging as promising carriers for the delivery of therapeutic biologics. Genetic engineering represents a robust strategy for loading proteins of interest into EVs. Identification of EV‐enriched proteins facilitates protein cargo loading efficiency. Many EV‐enriched proteins are sorted into EVs via an endosomal sorting complex required for transport (ESCRT)‐dependent pathway. In parallel, viruses hijack this EV biosynthesis machinery via conserved late domain motifs to promote egress from host cells. Inspired by the similarity of biogenesis between EVs and viruses, we developed a synthetic, Late domain‐based EV scaffold protein that enables the display of a set of single chain variable fragments (scFvs) on the EV surface. We named this scaffold the Late domain‐based exosomal antibody surface display platform (LEAP). We applied the LEAP scaffold to reprogramme HEK293T cell‐derived EVs to elicit T‐cell anti‐tumor immunity by simultaneously displaying αPD‐L1 and αCD3 scFvs on the EV surface (denoted as αPD‐L1×αCD3 bispecific T‐cell engaging exosomes, BiTExos). We demonstrated that αPD‐L1×αCD3 BiTExos actively redirected T cells to bind to PD‐L1+ tumor cells, promoting T‐cell activation, proliferation and tumoricidal cytokine production. Furthermore, the αPD‐L1×αCD3 BiTExos promoted T‐cell infiltration into the tumor microenvironment to mitigate the tumor burden in vivo. Our study suggested that the LEAP scaffold may serve as a platform for EV surface display and could be applied for a broad range of EV‐based biomedical applications. [ABSTRACT FROM AUTHOR]

Despite being some of the most anecdotally well‐known roads to pathogenesis, the mechanisms governing autoimmune rheumatic diseases are not yet fully understood. The overactivation of the cellular immune system and the characteristic development of autoantibodies have been linked to oxidative stress. Typical clinical manifestations, such as joint swelling and deformities and inflammation of the skin and internal organs, have also been connected directly or indirectly to redox mechanisms. The differences in generation and restraint of oxidative stress provide compelling evidence for the broad variety in pathology among rheumatic diseases and explain some of the common triggers and discordant manifestations in these diseases. Growing evidence of redox mechanisms in pathogenesis has provided a broad array of new potential therapeutic targets. Here, we explore the mechanisms by which oxidative stress is generated, explore its roles in autoimmunity and end‐organ damage, and discuss how individual rheumatic diseases exhibit unique features that offer targets for therapeutic interventions. [ABSTRACT FROM AUTHOR]

According to the latest evidence, the microbial metabolite Urolithin A (UA), known for its role in promoting cellular health, modulates CD8+ T cell‐mediated antitumor activity. However, the direct target protein of UA and its underlying mechanism remains unclear. Here, this research identifies ERK1/2 as the specific target crucial for UA‐mediated CD8+ T cell activation. Even at low doses, UA markedly enhances the persistence and effector functions of primary CD8+ cytotoxic T lymphocytes (CTLs) and human chimeric antigen receptor (CAR) T cells both in vitro and in vivo. Mechanistically, UA interacts directly with ERK1/2 kinases, enhancing their activation and subsequently facilitating T cell activation by engaging ULK1. The UA‐ERK1/2‐ULK1 axis promotes autophagic flux in CD8+ CTLs, enhancing cellular metabolism and maintaining reactive oxygen species (ROS) levels, as evidenced by increased oxygen consumption and extracellular acidification rates. UA‐treated CD8+ CTLs also display elevated ATP levels and enhanced spare respiratory capacity. Overall, UA activates ERK1/2, inducing autophagy and metabolic adaptation, showcasing its potential in tumor immunotherapy and interventions for diseases involving ERKs. [ABSTRACT FROM AUTHOR]

The barley powdery mildew fungus, Blumeria hordei (Bh), secretes hundreds of candidate secreted effector proteins (CSEPs) to facilitate pathogen infection and colonization. One of these, CSEP0008, is directly recognized by the barley nucleotide‐binding leucine‐rich‐repeat (NLR) receptor MLA1 and therefore is designated AVRA1. Here, we show that AVRA1 and the sequence‐unrelated Bh effector BEC1016 (CSEP0491) suppress immunity in barley. We used yeast two‐hybrid next‐generation interaction screens (Y2H‐NGIS), followed by binary Y2H and in planta protein–protein interactions studies, and identified a common barley target of AVRA1 and BEC1016, the endoplasmic reticulum (ER)‐localized J‐domain protein HvERdj3B. Silencing of this ER quality control (ERQC) protein increased Bh penetration. HvERdj3B is ER luminal, and we showed using split GFP that AVRA1 and BEC1016 translocate into the ER signal peptide‐independently. Overexpression of the two effectors impeded trafficking of a vacuolar marker through the ER; silencing of HvERdj3B also exhibited this same cellular phenotype, coinciding with the effectors targeting this ERQC component. Together, these results suggest that the barley innate immunity, preventing Bh entry into epidermal cells, requires ERQC. Here, the J‐domain protein HvERdj3B appears to be essential and can be regulated by AVRA1 and BEC1016. Plant disease resistance often occurs upon direct or indirect recognition of pathogen effectors by host NLR receptors. Previous work has shown that AVRA1 is directly recognized in the cytosol by the immune receptor MLA1. We speculate that the AVRA1 J‐domain target being inside the ER, where it is inapproachable by NLRs, has forced the plant to evolve this challenging direct recognition. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has affected 700 million people worldwide since its outbreak in 2019. The current pandemic strains, including Omicron and its large subvariant series, exhibit strong transmission and stealth. After entering the human body, the virus first infects nasal epithelial cells and invades host cells through the angiotensin‐converting enzyme 2 receptor and transmembrane serine protease 2 on the host cell surface. The nasal cavity is an important body part that protects against the virus. Immunisation of the nasal mucosa produces immunoglobulin A antibodies that effectively neutralise viruses. Saline nasal irrigation, a type of physical therapy, can reduce the viral load in the nasal cavity and prevent viral infections to some extent. As a commonly used means to fight SARS‐CoV‐2, the intramuscular (IM) vaccine can induce the human body to produce a systemic immune response and immunoglobulin G antibody; however, the antibody is difficult to distribute to the nasal mucosa in time and cannot achieve a good preventive effect. Intranasal (IN) vaccines compensate for the shortcomings of IM vaccines, induce mucosal immune responses, and have a better effect in preventing infection. In this review, we discuss the nasal defence barrier, the harm caused by SARS‐CoV‐2, the mechanism of its invasion into host cells, nasal cleaning, IM vaccines and IN vaccines, and suggest increasing the development of IN vaccines, and use of IN vaccines as a supplement to IM vaccines. [ABSTRACT FROM AUTHOR]

Background: Astaxanthin is the most prevalent carotenoid in the marine environment and is widely used as an additive in formulated aquafeeds. Objectives: A 60‐day feeding trial was conducted to consider the effect of dietary nanoliposome‐coated astaxanthin (NA) on haematological parameters, serum antioxidant activities and immune responses of rainbow trout, Oncorhynchus mykiss. Methods: A total of 450 healthy fish weighing 31.00 ± 2.09 g were randomly assigned in triplicate (30 fish per replicate) to 5 dietary treatments: 0 (control), 25.00, 50.00, 75.00, and 100.00 mg kg−1 NA. Results: Fish fed the diet supplemented with 50.00 mg kg−1 NA exhibited the highest values of red blood cells, white blood cells, haemoglobin and haematocrit of 1.64 ± 0.01 × 106 mm−3, 5.54 ± 0.21 × 103 mm−3, 8.73 ± 0.24 g dL−1 and 46.67% ± 0.88%, respectively, which were significantly higher than those fed the basal diet (p < 0.05). The lowest and highest percentages of lymphocytes (67.67% ± 0.33%) and neutrophils (27.33% ± 1.20%) were also obtained in fish fed 50.00 mg kg−1 NA compared to those fed the basal diet (p < 0.05). Fish receiving diet supplemented with 50.00 mg kg−1 NA revealed the highest serum activity in superoxide dismutase, catalase, glutathione peroxidase, lysozyme and alternative complement and the lowest level of total cholesterol, cortisol, aspartate aminotransferase and alanine aminotransferase than fish receiving the basal diet (p < 0.05). Serum immunoglobulin (Ig) and ACH50 contents significantly increased with increasing dietary NA supplementation to the highest values of 43.17 ± 1.46 and 293.33 ± 2.03 U mL−1, respectively, in fish fed diet supplemented with 50 mg kg−1 NA (p < 0.05). Conclusions: Supplementation of NA in rainbow trout diet at 50 mg kg−1 exhibited a positive effect on haematological parameters, antioxidant capacity and immune responses. Administration of such dosage can enhance rainbow trout immune responses against unfavourable or stressful conditions, for example disease outbreaks, hypoxic condition, thermal stress and sudden osmotic fluctuations, which usually happen in an intensive culture system. [ABSTRACT FROM AUTHOR]

Sonesson M, Ericson D, Kinnby B, Wickström C. Glycoprotein 340 and sialic acid in minor-gland and whole saliva of children, adolescents, and adults. Eur J Oral Sci 2011; 119: 435-440. © 2011 Eur J Oral Sci Glycoprotein 340 (gp-340) is a bacterial-binding glycoprotein found in major-gland and minor-gland saliva. Sialic acid, a common terminal structure of salivary glycoproteins, interacts with microorganisms and host ligands, as well as with free radicals. This study investigated the contents of gp-340 and sialic acid in minor-gland saliva and whole saliva of children (3 yr of age), adolescents (14 yr of age), and adults (20-25 yr of age). Labial-gland saliva and buccal-gland saliva were collected on filter paper, and unstimulated whole saliva was collected by draining into a tube. The relative amount of gp-340 and sialic acid was determined by ELISA and by enzyme-linked lectin assay (ELLA), respectively. In minor-gland saliva, no statistically significant differences in gp-340 and sialic acid were seen between the age-groups. Among adults, significantly lower amounts of gp-340 and sialic acid were seen in labial saliva compared with buccal saliva. In whole saliva, the amount of gp-340 was significantly lower among adults compared with children. No differences between genders were seen. Stable content of gp-340 and sialic acid in minor-gland saliva across the age-groups, and a higher content of gp-340 in the whole saliva of the youngest age-group (3-yr-olds) compared with the adult group, may reflect that those components are vital innate factors of immunity in children's saliva. [ABSTRACT FROM AUTHOR]

The digestive tract works through a complex network of integrative functions. At the level of the gut, this integration occurs between the immune, neuromotor and enteroendocrine systems, coordinating the physical and chemical elements of the intestinal barrier in order to facilitate digestion whilst protecting the gut from unwanted components of the luminal contents. Gastrointestinal function is controlled and coordinated by the central nervous system to ensure effective motility, secretion, absorption and mucosal immunity. It follows that perturbations in this complex network could lead to gut dysfunction and symptom generation. Recently, attention has been focused on the emerging hypothesis that gut luminal content contributes to determine normal GI function and on the therapeutic possibilities arising from modulating its impact on gut physiology and immunity using probiotic bacteria. In this issue of Neurogastroenterology and Motility, two papers explore the effect of specific probiotic bacteria on spinal neuronal activation and in vitro muscle contractility. These papers support the notion that the composition of the intestinal microbiota can influence gut neuro-motor function and enhance our understanding on the mechanisms of action underlying the effects of specific probiotics on gut functional disorders. [ABSTRACT FROM AUTHOR]

Summary: The concept of trained immunity refers to remodelling of the monocyte and macrophage metabolic and epigenetic landscape, conferring an amplified inflammatory response upon secondary stimulation. This effect is typically modelled in vitro by stimulating monocytes with either Bacillus Calmette Guerin (BCG) or β‐Glucan for 24 hr, before subsequent stimulation with LPS or Pam‐3‐Cys (P3C) as a secondary stimulus 6 days later. Here, we focus on a recent paper which interrogated the role of the anti‐inflammatory TLR, TLR10, on trained immunity. Using both an in vitro model of trained immunity, and analysis of BCG vaccinated individuals, the authors interestingly demonstrate that, despite its ability to regulate aspects of innate immunity, TLR10 does not have a significant role in this process. [ABSTRACT FROM AUTHOR]

Summary: This paper discusses the following ten subtitles with the contents indicated. 1. To meet a microbe: discusses the four alternatives in host-microbe interactions. 2. Receptors and signal transduction giving gene activation: discusses the lipopolysaccharide receptor and the limitations of cell cultures versus use of live animals. 3. Effector molecules -- antimicrobial peptides with and without cysteines. A data base exists with over 500 sequences. This paper gives a general overview of five classes of gene-encoded effector molecules, based on the absence or presence of cysteines. These molecules are peptide antibiotics with wide spectra against different microbes. They are synthesized as propeptides and post-translational modifications are common. 4. Effectors of innate immunity -- lethal action without host damage: evaluates current opinions about the mode of action of peptide antibiotics and the fact that these effectors do not create host damage. 5. Genes, introns and movable elements. Two cecropin genes containing movable elements and the human cathelicidin gene for proFALL-39/hCAP18 are discussed. 6. The natural microflora. Hippos or frogs as model systems. This section includes the isolation of bacteria from the normal flora of frogs; Aeromonas hydrophila, the bacterium found on all five frog species studied; arguments and selected examples of frog-microbe interactions in vivo and in vitro; and the use of glucocorticoids as control for nuclear factor-κB/IκBα regulation of effector genes. 7. The use of germ-free mice -- hard facts from hard work: summarizes new findings which indicate that germ-free mice are born with a seat of antibacterial peptides in their small intestine. The intestine of germ-free mice monoinfected with A. hydrophila have peptide patterns that differ depending on a pretreatment with cortisone. 8. Looking... [ABSTRACT FROM AUTHOR]

We are not merely talking about a blank immune population needing urgent vaccination but of a complex milieu of immunized subjects, whose thorough and expert knowledge may provide fundamental insights to improve the management of COVID-19 pandemic emergency. Escaping from COVID-19 emergency accounting on previously infected subjects? In a recent paper, some authors wondered if the COVID-19 pandemic will end with the Omicron (B.1.1.529) and Delta (B.1.617.2) variants.1 The variant of concern (VoC) Omicron is characterized by few some deletions and more than 30 mutations, several of which (e.g., 69-70del, T95I, G142D/143-145del, K417N, T478K, N501Y, N655Y, N679K, and P681H) overlapping with those ones retrievable in the Alpha, Beta, Gamma, or Delta VoCs.2 This enables the B.1.1.529 VoC to break through existing vaccines, escape vaccine-induced vaccination, and widespread very rapidly, though with a very poor lethality. [Extracted from the article]

Our understanding of immunity to filarial infection is enigmatic and continues to be passionately debated. The mechanisms whereby filarial nematodes are killed in vivo and how these parasites avoid these mechanisms are poorly understood. Although vaccination studies in permissive animals took off seven decades ago, the exact mechanisms driving protective immunity are extensively being investigated. Currently, little is known regarding the collective functions or counter-regulatory mechanisms of the antibody isotypes in filarial infection with respect to protective immunity. Establishing the functional role of antibody isotypes and cytokines in the various infection phenotypes can contribute immensely to current knowledge in filarial immunology. This paper reviews insight into protective immunity in filarial infection with focus on humoral and cellular responses from animal models and human studies. [ABSTRACT FROM AUTHOR]

Several hybridoma cell lines secreting NP-specific, murine IgE antibodies were generated by fusion of P3-X20 (γ,κ) tumour cells with spleen cells from (BALB/c x C57Bl/6)F1 (CB6F1) mice previously immunized with NP-ovalbumin. Four subclones (designated NP-ε-3.57, NP-ε-15,88, NP-ε-91,58 and NP-ε-95,31) were propagated in vivo and milligram quantities of the corresponding IgE antibodies were purified from ascitic fluid by gel filtration, ion exchange chromatography and affinity chromatography. Immunological analyses and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDSPAGE) indicated that NP-ε-15,88, NP-ε-91,58 and NP-ε-95.31 all possessed λ1 (or possibly λ3) light chains; and that NP-ε-3,57 possessed λ2 light chains; NP-&elipson;-95,31 also expressed the P3-X20 derived, MOPC-21 κ light chain. Radioallergosorbent test (RAST) titration curves, generated from the interaction of the four monoclonal IgE antibodies with NP-BSA attached to paper discs (NP-BSA-P) were found to be non-overlapping. Measurements of the relative amounts of NP-ε-aminocaproic acid (NP-CAP) and 4-hydro-3-iodo-5-nitrophenylacetyl-ε- aminocaproic acid (NIP-CAP) that were required to inhibit by 50% the binding of the 4 IgE antibodies to NP-BSA-P indicated that these antibodies were all heteroclitic, since their affinity for NIP appeared to be higher than their affinity for NP. These results, in conjunction with other findings reported in the literature, suggested that the V regions of NP-specific IgE antibodies are similar to the V regions of NP-specific IgM and IgG antibodies, produced by the same mouse strains. Finally, in vitro histamine release measurements demonstrated that two of these monoclonal IgE antibodies could mediate antigen induced histamine release from passively sensitized rat peritoneal mast cells. [ABSTRACT FROM AUTHOR]

Protective immunity against mycobacteria is dependent on antigen-specific T cells. The antibodies induced upon immunization with mycobacteria have no apparent role in host protection, Serological techniques have detected some antigens that are also recognized by human T cells but may fail to recognize others. Potentially, there may be differences in the epitopes seen by the T and B cell anti-mycobacterial antigen repertoires. We have screened the different components of sonicated BCG or Mycobacterium leprae that were separated according to their molecular weight (MW) by SDS-PAGE and then electroblotted on nitrocellulose paper. The blots were cut into squares and tested directly in a T cell proliferation assay. Our results indicate that peripheral T cells of healthy leprosy patient contacts respond preferentially to the lower MW (<70,000) and not the higher MW fractions of M. leprae and BCG, in contrast to the humoral response of these same individuals. The most important fractions in inducing a lymphoproliferative response were in the regions of 11-16 kDa of BCG and M. leprae and to the 22-26 kDa region of M. leprae. These fractions appeared to represent molecular weight regions that were in some instances clearly distinct from previously defined antigens. It was further shown that lymphoproliferation in response to mycobacterial fractions correlated with the production of gamma interferon, a lymphokine required for macrophage activation and elimination of mycobacteria. These studios allow the direct assessment of antigens involved in protective T cell-mediated immunity, and should be helpful in selecting relevant antigens for skin testing and immunization. [ABSTRACT FROM AUTHOR]

The article presents various abstracts on different papers on allergy, immunity, tumors, hereditary and infectious diseases. Some of the papers are "Biologic and immunomodulating factors in the treatment of pediatric acquired immunodeficiency syndrome," "Presence of human immunodeficiency syndrome in laser smoke," "Disseminated mucormycosis in an infant with methylmalonicaciduria," "Comparison of mupicorin and erythromycin in the treatment of impetigo," and "Flashlamp-pumped pulsed dye laser for port-wine stains in infancy: earlier versus later treatment."