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Dendritic cells (DCs) are essential for initiating immune responses. Depending on the environment, the type of DC and the way in which they interact with T cells, these immune responses can be beneficial or detrimental. DCs can be exploited as cellular vectors for vaccines against infection and cancer. The development and maintenance of DCs is dependent on the FMS‐like tyrosine kinase 3 (Flt3)/Flt3 ligand (Flt3L) signaling cascade. Flt3 is also one of the most commonly mutated genes in acute myeloid leukemia and as such represents an attractive drug target. In this review, Flt3 is discussed with a particular focus on DCs. We detail the lifecycle of Flt3, from transcription to degradation, and interrogate recent studies as to how this pathway can be manipulated for immunotherapy, vaccination and treatment of autoimmune disease. [ABSTRACT FROM AUTHOR]

There is growing interest in understanding antibody (Ab) function beyond neutralization. The non‐structural protein 1 (NS1) of Zika virus (ZIKV) is an attractive candidate for an effective vaccine as Abs against NS1, unlike the envelope or premembrane, do not carry the risk of mediating antibody‐dependent enhancement. Our aim was to evaluate whether ZIKV NS1 Abs elicited following natural infection in humans can mediate antibody‐dependent cellular cytotoxicity (ADCC). We evaluated the isotype specificity of ZIKV‐specific Abs in immune sera and supernatants from stimulated immune PBMC and found that Abs against ZIKV NS1 and virus‐like particles were predominantly of the IgG1 isotype. Using a recently developed FluoroSpot assay, we found robust frequencies of NS1‐specific Ab‐secreting cells in PBMC of individuals who were naturally infected with ZIKV. We developed assays to measure both natural killer cell activation by flow cytometry and target cell lysis of ZIKV NS1‐expressing cells using an image cytometry assay in the presence of ZIKV NS1 Abs. Our data indicate efficient opsonization of ZIKV NS1‐expressing CEM‐NKR cell lines using ZIKV‐immune but not ZIKV‐naïve sera, a prerequisite of ADCC. Furthermore, sera from immune donors were able to induce both NK cell degranulation and lysis of ZIKV NS1 CEM‐NKR cells in vitro. Our data suggest that ADCC is a possible mechanism for ZIKV NS1 Abs to eliminate virally infected target cells. [ABSTRACT FROM AUTHOR]

Presents abstracts of research papers on immunity and repair in the nervous system, published in the December 2002 supplement of 'Immunology.' 'The Immunobiology of TSE diseases,' by N.A. Mabbott; 'Autoimmunity in the peripheral nervous system: An overview,' by H.J. Willison.

SUMMARY: The oomycete Albugo candida causes white rust of Brassicaceae, including vegetable and oilseed crops, and wild relatives such as Arabidopsis thaliana. Novel White Rust Resistance (WRR) genes from Arabidopsis enable new insights into plant/parasite co‐evolution. WRR4A from Arabidopsis accession Columbia (Col‐0) provides resistance to many but not all white rust races, and encodes a nucleotide‐binding, leucine‐rich repeat immune receptor. Col‐0 WRR4A resistance is broken by AcEx1, an isolate of A. candida. We identified an allele of WRR4A in Arabidopsis accession Øystese‐0 (Oy‐0) and other accessions that confers full resistance to AcEx1. WRR4AOy‐0 carries a C‐terminal extension required for recognition of AcEx1, but reduces recognition of several effectors recognized by the WRR4ACol‐0 allele. WRR4AOy‐0 confers full resistance to AcEx1 when expressed in the oilseed crop Camelina sativa. [ABSTRACT FROM AUTHOR]

The deterioration of tissue structure and decline in physiological function during aging are accompanied by alterations to the gut microbiota. The elderly has higher risks of various diseases and chronic diseases. However, inter‐individual differences are more apparent in elderly than younger, and a proportion of individuals have a delayed onset or even avoid developing chronic diseases. This difference in health status is influenced by both heredity and Lifestyle and environmental factors. During the process of aging, the gut microbiota is also affected by the external environment, and provides a buffer to external challenge, and thus the gut microbiota reflects an individual's personal experience. Moreover, the immune system undergoes a series of changes with age, which are related to chronic inflammation in the elderly. The formation, maturation and senescence of the intestinal immune system is closely related to the gut microbiota. Additionally, changes in the gut microbiota of elderly individuals may modulate the immune system, which may in turn affect health status. Herein, we summarize the correlations between the gut microbiota with individual health status in the elderly and explore the related mechanisms, which may provide a basis to maintain or enhance the health of the elderly though interventions targeting the gut microbiota. [ABSTRACT FROM AUTHOR]

Background: Toll‐interacting protein is a key factor in regulating innate immunity responses via gatekeeping Toll‐like receptors. Genetic variance in innate immunity has been linked with susceptibility to infections. Children with viral bronchiolitis in infancy are at increased risk of later asthma. The aim was to evaluate the role of toll‐interacting protein gene point mutations in severity of bronchiolitis and subsequent risk of asthma. Methods: Infants less than 6 months old were recruited during hospitalization due to bronchiolitis. In all, 166 children were prospectively followed up to age of 1.5, 6, and 11 years. Clinical data on viral etiology and severity markers, and further post‐bronchiolitis asthma and lung function outcomes were compared with genetic differences in two single‐nucleotide point mutations rs116938768 and rs5743854 in the toll‐interacting protein gene. Results: Toll‐interacting protein rs116938768 or rs5743854 did not show significant associations with severity markers or viral etiology of bronchiolitis. Follow‐up data on current asthma or lung function at 6 or 11 years of age after bronchiolitis were not associated with the investigated mutations. Conclusion: Toll‐interacting protein gene point mutations in rs116938768 or rs5743854 were not involved with the clinical course of viral bronchiolitis in early infancy, and did not predict post‐bronchiolitis asthma or lung function reduction by the age of 11 years. [ABSTRACT FROM AUTHOR]

Background: Glomerular endothelial cells (GECs) are directly exposed to circulating viral particles in the glomerulus. Although viral infections may trigger the development of acute kidney injury or the worsening of pre‐existing chronic kidney disease, the specific molecular mechanisms underlying antiviral reactions via the activation of endothelial Toll‐like receptor 3 signaling in the kidney remain to be determined. Interferon (IFN)‐induced transmembrane protein 1 (IFITM1), a member of interferon‐stimulated gene protein family, is involved in the prevention of viral entry into cerebral vascular endothelial cells, respiratory epithelial cells, and endometrium. However, as far as we are aware, the implication of IFITM1 associated with viral infections in GECs has not been investigated to date. Methods: Cultured, normal human GECs were treated with polyinosinic‐polycytidylic acid (poly IC), a synthesized viral double‐stranded RNA, then the expression of IFITM1 was examined by quantitative real‐time reverse transcription‐polymerase chain reaction and western blotting. To further elucidate the poly IC‐induced signaling pathway, the cells were applied to RNA interference against IFN‐β, nuclear factor‐κB p65, and IFN regulatory factor 3. We also conducted an immunofluorescence study to examine endothelial IFITM1 expression in biopsy specimens from patients with chronic kidney disease. Results: We found that the activation of Toll‐like receptor 3 induced endothelial expression of IFITM1, and that this involved IFN regulatory factor 3 and IFN‐β, but not nuclear factor‐κB. Intense endothelial IFITM1 immunoreactivity was observed in biopsy specimens from patients with lupus nephritis. Conclusions: Antiviral reaction‐related endothelial expression of IFITM1 may be involved, at least in part, in the development of particularly in lupus nephritis. Further detailed studies of the implication of interferon stimulated genes, including IFITM1 in GECs are needed. [ABSTRACT FROM AUTHOR]

Many aphid‐vectored viruses are transmitted nonpersistently via transient attachment of virus particles to aphid mouthparts and are most effectively acquired or transmitted during brief stylet punctures of epidermal cells. In Arabidopsis thaliana, the aphid‐transmitted virus cucumber mosaic virus (CMV) induces feeding deterrence against the polyphagous aphid Myzus persicae. This form of resistance inhibits prolonged phloem feeding but promotes virus acquisition by aphids because it encourages probing of plant epidermal cells. When aphids are confined on CMV‐infected plants, feeding deterrence reduces their growth and reproduction. We found that CMV‐induced inhibition of growth as well as CMV‐induced inhibition of reproduction of M. persicae are dependent upon jasmonate‐mediated signalling. BRASSINOSTEROID INSENSITIVE1‐ASSOCIATED KINASE1 (BAK1) is a co‐receptor enabling detection of microbe‐associated molecular patterns and induction of pattern‐triggered immunity (PTI). In plants carrying the mutant bak1‐5 allele, CMV induced inhibition of M. persicae reproduction but not inhibition of aphid growth. We conclude that in wildtype plants CMV induces two mechanisms that diminish performance of M. persicae: a jasmonate‐dependent and PTI‐dependent mechanism that inhibits aphid growth, and a jasmonate‐dependent, PTI‐independent mechanism that inhibits reproduction. The growth of two crucifer specialist aphids, Lipaphis erysimi and Brevicoryne brassicae, was not affected when confined on CMV‐infected A. thaliana. However, B. brassicae reproduction was inhibited on CMV‐infected plants. This suggests that in A. thaliana CMV‐induced resistance to aphids, which is thought to incentivize virus vectoring, has greater effects on polyphagous than on crucifer specialist aphids. [ABSTRACT FROM AUTHOR]

Aim: The aim of the study was to assess the effect of changes in population size and migration on variation in functional immunity genes in the previously bottlenecked population of the grey wolf, Canis lupus. Location: Eastern/Central Europe: Poland, Czechia, Slovakia. Methods: We genotyped 7 immunity genes: three MHC‐DLA genes (dog leukocyte antigen) and four Toll‐like receptor (TLR) genes among 130 wolves originating from three populations: two lowland (Baltic and Central European), and highland Carpathian. We contrasted the population structure in immunity genes with a neutral structure based on 13 microsatellites, and we analysed signatures of selection in the immunity loci. Results: We found high overall genetic variance in immunity genes and no evidence for decreased diversity in the recently established populations. The population structure in immunity loci was weak, with pairwise FST lower than for neutral markers. Although the results of neutrality tests were not significant, we identified codons under selection, both positive and negative. Main Conclusions: We demonstrated that despite recent population expansion which is expected to result in decreased genetic diversity, the diversity of immunity genes in the newly established wolf population is similar to those in the source population. This suggests that migrations do not cause allele loss in grey wolf. Signatures of selection on codon level, but not in tests using allele frequencies, suggest the contrasting effects of demography and selection. [ABSTRACT FROM AUTHOR]

Mitochondrial antiviral signaling (MAVS) protein is the core signaling adaptor in the RNA signaling pathway. Thus, appropriate regulation of MAVS expression is essential for antiviral immunity against RNA virus infection. However, the regulation of MAVS expression at the mRNA level especially at the post transcriptional level is not well‐defined. Here, it is reported that the MAVS mRNA undergoes N6‐methyladenosine (m6A) modification through methyltransferase‐like protein 14 (METTL14), which leads to a fast turnover of MAVS mRNA. Knockdown or deficiency of METTL14 increases MAVS mRNA stability, and downstream phosphorylation of TBK1/IRF3 and interferon‐β production in response to RNA viruses. Compared to wild‐type mice, heterozygotes Mettl14+/− mice better tolerate RNA virus infection. The authors' findings unveil a novel mechanism to regulate the stability of MAVS transcripts post‐transcriptionally through m6A modification. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to assess associations between neutrophil‐related primary immunodeficiencies (PIDs) and the presence of periodontal disease and other oral diseases and response to periodontal treatment. Background: Presence of neutrophil‐related PIDs is thought to be a major risk factor for development of periodontitis. Methods: This study had both a cross‐sectional and cohort design. Twenty‐four children (age 4–16) with PIDs and 24 age‐matched systemically healthy subjects received a dental clinical examination, including measures of probing pocket depths (PPD), clinical attachment loss (CAL) and bleeding on probing (BOP). Those found to be affected by periodontal disease were offered periodontal treatment and reassessed 6 months later. Results: Diagnosis of PIDs was associated with increased odds of presence of periodontal disease (p =.008 adjusted for age, gender, plaque, OR = 10.0, 95% CI = 1.83–54.38) and with continuous measures of periodontal disease such as number of PPDs >4 mm, mean PPD and mean CAL (all p <.001) and BOP (p =.001). However, only 7 out of 24 children were diagnosed with periodontitis. PIDs were also associated with a history of oral ulcers (p =.001, OR 12.47, 95% CI 2.71–57.29). An improvement in periodontal parameters (PPD and CAL) was detected following oral hygiene instructions and non‐surgical periodontal therapy. Conclusion: Although children affected by neutrophil‐associated PIDs exhibited a higher prevalence of periodontal disease compared with systemically healthy children, severe periodontitis was rarely seen. This suggests that good systemic control of the PIDs may reduce their impact on the periodontium. [ABSTRACT FROM AUTHOR]

Research suggests that emerging information about infection‐acquired COVID‐19 immunity should be interpreted with caution. The introduction of "immunity passports" that would enable people who have recovered from COVID‐19 to travel freely and return to work may therefore have detrimental consequences if not managed carefully. In two studies, we examined how perceived (suspected or imagined) recovery from COVID‐19, and the concept of immunity passports, influence people's intentions to engage in behaviors aimed to reduce the spread of COVID‐19. We also consider ways to lessen potential negative effects. In Study 1 (N = 1604), participants asked to imagine that they had recovered from COVID‐19 reported lower social distancing intentions compared to a control condition. Participants who suspected (versus imagined) that they had recovered from past infection did not report lower preventative intentions compared to the control condition, even at high levels of certainty of past infection. In Study 2 (N = 1732), introducing the idea of immunity passports also reduced social distancing intentions compared to a control condition. The latter effect was, however, attenuated when cautious information about the equivocal science on COVID‐19 was also presented to participants. Participants who suspected that they had COVID‐19 in the past (compared to the control condition) revealed a similar pattern of results, but only at higher levels of certainty of past infection. Caution regarding infection‐acquired COVID‐19 immunity and immunity passports will be crucial in the COVID‐19 response. Implications for premature pandemic announcements, as well as their potential remedies, are discussed. [ABSTRACT FROM AUTHOR]

Objective: The loss of LOXL1 expression reportedly leads to the prolapse of pelvic organs or to exfoliation syndrome glaucoma. Increasing evidence suggests that LOXL1 deficiency is associated with the pathogenesis of several other diseases. However, the characterization of the systemic functions of LOXL1 is limited by the lack of relevant investigative technologies. Materials and Methods: To determine the functions of LOXL1, a novel method for body‐wide organ transcriptome profiling, combined with single‐cell mass cytometry, was developed. A body‐wide organ transcriptomic (BOT) map was created by RNA‐Seq of tissues from 17 organs from both Loxl1 knockout (KO) and wild‐type mice. Results: The BOT results indicated the systemic upregulation of genes encoding proteins associated with the immune response and proliferation processes in multiple tissues of KO mice, and histological and immune staining confirmed the hyperplasia and infiltration of local immune cells in the tissues of KO mice. Furthermore, mass cytometry analysis of peripheral blood samples revealed systemic immune changes in KO mice. These findings were well correlated with results obtained from cancer databases. Patients with tumours had higher Loxl1 mutation frequencies, and patients with Loxl1‐mutant tumours showed the upregulation of immune processes and cell proliferation and lower survival rates. Conclusion: This study provides an effective strategy for the screening of gene functions in multiple organs and also illustrates the important biological roles of LOXL1 in the cells of multiple organs as well as in systemic immunity. [ABSTRACT FROM AUTHOR]

The trial was aimed at evaluating probable superiority, if any of nano zinc (NZn) over inorganic zinc (Zn) on immunity, serum minerals and T3, T4, and IGF-1 hormone profiles in goats. NZn was synthesized by using 0.45 M aqueous solution of Zn nitrate and 0.9 M aqueous solution of sodium hydroxide (average particle size 74 nm). Twenty-four male goats were grouped into four groups as per their body weight and were supplemented with either a basal diet with concentrate and straw at 50:50 ratio (Negative control, NC) alone or supplemented with 50 mg/kg Zn (Control) from inorganic Zn source, that is ZnO (IZn-50), 50 mg/kg Zn from NZn (NZn-50) or 25 mg/kg Zn from NZn (NZn-25). No change was observed in thyroid hormone status on zero and 90th day of experimental feeding, but NZn supplementation improved (p < 0.05) IGF-1 level on 90th day serum samples. Zn supplementation improved the humoral immunity in all the groups irrespective of the source. Similarly, cell-mediated immunity (CMI) measured by skinfold thickness after injecting Con-A, was also improved in Zn supplemented groups than control at 6, 12 and 48 h of incubation. NZn-50 animals showed highest HI (haemagglutination inhibition) titre as well as skin thickness. The CD+ 4 (cluster of differentiation in %) was more (p < 0.05) in Zn supplemented groups. NZn-50 showed higher (p < 0.05) CD+ 8 among the treatment groups. Thus, NZn supplementation at 25 mg/kg had similar immunity and serum T+ 4, CD+ 8 among the treatment groups. Thus, NZn supplementation at 25 mg/kg had similar immunity and serum T3, T4 and IGF-1 profiles compared with IZn at 50 mg/kg dose. [ABSTRACT FROM AUTHOR]

Plants employ systemic‐induced resistance as part of their defence arsenal against pathogens. In recent years, the application of mild heating has been found to induce resistance against several pathogens. In the present study, we investigated the effect of root zone warming (RZW) in promoting tomato's resistance against the necrotrophic fungus Botrytis cinerea (Bc), the hemibiotrophic bacterium Xanthomonas campestris pv. vesicatoria (Xcv) and the biotrophic fungus Oidium neolycopersici (On). We demonstrate that RZW enhances tomato's resistance to Bc, On and Xcv through a process that is dependent on salicylic acid and ethylene. RZW induced tomato immunity, resulting in increased defence gene expression, reactive oxygen species (ROS) and ethylene output when plants were challenged, even in the absence of pathogens. Overall, the results provide novel insights into the underlying mechanisms of warming‐induced immune responses against phytopathogens with different lifestyles in tomato. Plants are often exposed to several stresses simultaneously, particularly in agricultural settings; here, we investigate the relationships between heat and pathogen stresses. We demonstrate that root zone warming induces systemic immunity and promotes resistance to several tomato pathogens, through a process that is dependent on salicylic acid and ethylene. [ABSTRACT FROM AUTHOR]

Salamanders exhibit the most extensive regenerative repertoire among vertebrates, being able to accomplish scar‐free healing and faithful regeneration of significant parts of the eye, heart, brain, spinal cord, jaws and gills, as well as entire appendages throughout life. The cellular and molecular mechanisms underlying salamander regeneration are currently under extensive examination, with the hope of identifying the key drivers in each context, understanding interspecies differences in regenerative capacity, and harnessing this knowledge in therapeutic settings. The immune system has recently emerged as a potentially critical player in regenerative responses. Components of both innate and adaptive immunity have been found at critical stages of regeneration in a range of salamander tissues. Moreover, functional studies have identified a requirement for macrophages during heart and limb regeneration. However, our knowledge of salamander immunity remains scarce, and a thorough definition of the precise roles played by its members is lacking. Here, we examine the evidence supporting roles for immunity in various salamander regeneration models. We pinpoint observations that need revisiting through modern genetic approaches, uncover knowledge gaps, and highlight insights from various model organisms that could guide future explorations toward an understanding of the functions of immunity in regeneration. Key Findings: We revisit research on the role of immunity in salamander regeneration from various speciesWe present a comparative analysis with other model vertebratesWe uncover knowledge gaps, propose new research avenues and highlight findings that should be scrutinised using state‐of‐the‐art genetic approaches [ABSTRACT FROM AUTHOR]

Summary: Serum amyloid A (SAA) is an acute‐phase protein (APP) to which multiple immunological functions have been attributed. Regardless, the true biological role of SAA remains poorly understood. SAA is remarkably conserved in mammalian evolution, thereby suggesting an important biological function. Since its discovery in the 1970s, the majority of researchers have investigated SAA using recombinant forms made available through bacterial expression. Nevertheless, recent studies indicate that these recombinant forms of SAA are unreliable. Indeed, commercial SAA variants have been shown to be contaminated with bacterial products including lipopolysaccharides and lipoproteins. As such, biological activities and receptor usage (TLR2, TLR4) revealed through the use of commercial SAA variants may not reflect the inherent nature of this APP. Within this review, we discuss the biological effects of SAA that have been demonstrated through more solid experimental approaches. SAA takes part in the innate immune response via the recruitment of leucocytes and executes, through pathogen recognition, antimicrobial activity. Knockout animal models implicate SAA in a range of functions, such as regulation of T‐cell‐mediated responses and monopoiesis. Moreover, through its structural motifs, not only does SAA function as an extracellular matrix protein, but it also binds extracellular matrix proteins. Finally, we here also provide an overview of definite SAA receptor‐mediated functions and highlight those that are yet to be validated. The role of FPR2 in SAA‐mediated leucocyte recruitment has been confirmed; nevertheless, SAA has been linked to a range of other receptors including CD36, SR‐BI/II, RAGE and P2RX7. [ABSTRACT FROM AUTHOR]

Periodontitis, caused by infection with periodontal pathogens, is primarily characterized by inflammatory bone resorption and destruction of connective tissue. Simply describing periodontitis as a specific bacterial infection cannot completely explain the various periodontal tissue destruction patterns observed. Periodontal tissue damage is thought to be caused by various factors. In recent years, research goals for periodontal pathogens have shifted from searching for specific pathogens to investigating mechanisms that damage periodontal tissues. Bacteria interact directly with the host in several ways, influencing expression and activity of molecules that evade host defenses, and destroying local tissues and inhibiting their repair. The host's innate and acquired immune systems are important defense mechanisms that protect periodontal tissues from attack and invasion of periodontal pathogens, thus preventing infection. Innate and acquired immunity have evolved to confront the microbial challenge, forming a seamless defense network in periodontal tissues. In the innate immune response, host cells quickly detect, via specialized receptors, macromolecules and nucleic acids present on bacterial cell walls, and this triggers a protective, inflammatory response. The work of this subsystem of host immunity is performed mainly by phagocytes, beta-defensin, and the complement system. In addition, the first line of defense in oral innate immunity is the junctional epithelium, which acts as a physical barrier to the entry of oral bacteria and other nonself substances. In the presence of a normal flora, junctional epithelial cells differentiate actively and proliferate apically, with concomitant increase in chemotactic factor expression recruiting neutrophils. These immune cells play an important role in maintaining homeostasis and the protective state in periodontal tissue because they eliminate unwanted bacteria over time. Previous studies indicate a mechanism for attracting immune cells to periodontal tissue with the purpose of maintaining a protective state; although this mechanism can function without bacteria, it is enhanced by the normal flora. A better understanding of the relationship between the protective state and its disruption in periodontal disease could lead to the development of new treatment strategies for periodontal disease. [ABSTRACT FROM AUTHOR]

Background: Protecting against CMV infection and maintaining CMV in latent state are largely provided by CMV‐specific T‐cells in lung transplant recipients. The aim of the study was to assess whether a specific T‐cell response is associated with the risk for CMV infection in seronegative patients who are at high risk for delayed CMV infection. Methods: All CMV‐seronegative recipients (R−) from CMV‐seropositive donors (D+) between January 2018 and April 2019 were included and retrospectively screened for CMV infection before and after assessment of CMV‐specific cell‐mediated immunity. Results: Thirty‐one of the 50 patients (62%) developed early‐onset CMV infection. Lower absolute neutrophil counts were significantly associated with early‐onset CMV infection. Antiviral prophylaxis was ceased after 137.2 ± 42.8 days. CMV‐CMI were measured at a median of 5.5 months after LTx. 19 patients experienced early and late‐onset CMV infection after prophylaxis withdrawal within 15 months post transplantation. Positive CMV‐CMI was significantly associated with lower risk of late‐onset CMV infection after transplantation in logistic and cox‐regression analysis (OR=0.05, p =.01; OR=2,369, p =.026). Conclusion: D+/R− lung transplant recipients are at high risk of developing early and late‐onset CMV infection. Measurement of CMV‐CMI soon after transplantation might further define the CMV infection prediction risk in LTx recipients being at high risk for CMV viremia. [ABSTRACT FROM AUTHOR]

Low vaccine immunogenicity and tumor heterogenicity greatly limit the therapeutic effect of tumor vaccine. In this study, a novel injectable adhesive hydrogel, based on thermosensitive nanogels containing catechol groups and loaded with in situ‐forming MnO2 nanoparticles, is constructed to overcome these issues. The concentrated nanogel dispersion transforms into an adhesive hydrogel in situ after intratumoral injection. The photothermal effect of the loaded MnO2 nanoparticles induces immunogenic cell death to release mass autologous tumor‐derived protein antigens under near‐infrared irradiation, which act as ideal immune stimulating substances avoiding the problem of tumor heterogenicity and are captured by the in situ‐forming adhesive hydrogel. The antigens‐captured adhesive hydrogel acts as an "antigen reservoir" and releases these captured antigens to recruit more dendritic cells to stimulate an intensive and lasting anti‐tumor immune response mediated by CD8+ T cells. The primary tumors can be almost completely disappeared within 4 days without relapse, and the growth of the distal tumors and rechallenged tumors are also effectively inhibited by the treatment with the injectable adhesive hydrogel‐based photothermal therapy. Therefore, the proposed "antigen reservoir" strategy shows the great potential application as an in situ‐forming personalized vaccine to enhancing the cancer immune therapy. [ABSTRACT FROM AUTHOR]

Evidence of robust memory T-cell responses in patients with chronic myeloproliferative neoplasms following infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) Keywords: COVID-19; immunity; T cell; myeloproliferative neoplasm; CML EN COVID-19 immunity T cell myeloproliferative neoplasm CML 692 696 5 05/17/21 20210515 NES 210515 Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a novel coronavirus, has led to very significant global healthcare challenges. Patients with chronic MPN without detectable antibodies had a T-cell response that was broadly equivalent in many areas to that seen in those with detectable anti-SARS-CoV-2 antibodies. For the first time, we have demonstrated that patients with chronic MPN can mount functional memory T-cell responses following natural SARS-CoV-2 exposure. [Extracted from the article]

Summary: Mycobacterium ulcerans causes Buruli ulcer, a neglected tropical skin disease manifesting as chronic wounds that can leave victims with major, life‐long deformity and disability. Differently from other mycobacterial pathogens, M ulcerans produces mycolactone, a diffusible lipid factor with unique cytotoxic and immunomodulatory properties. Both traits result from mycolactone targeting Sec61, the entry point of the secretory pathway in eukaryotic cells. By inhibiting Sec61, mycolactone prevents the host cell's production of secreted proteins, and most of its transmembrane proteins. This molecular blockade dramatically alters the functions of immune cells, thereby the generation of protective immunity. Moreover, sustained inhibition of Sec61 triggers proteotoxic stress responses leading to apoptotic cell death, which can stimulate vigorous immune responses. The dynamics of bacterial production of mycolactone and elimination by infected hosts thus critically determine the balance between its immunostimulatory and immunosuppressive effects. Following an introduction summarizing the essential information on Buruli ulcer disease, this review focuses on the current state of knowledge regarding mycolactone's regulation and biodistribution. We then detail the consequences of mycolactone‐mediated Sec61 blockade on initiation and maintenance of innate and adaptive immune responses. Finally, we discuss the key questions to address in order to improve immunity to M ulcerans, and how increased knowledge of mycolactone biology may pave the way to innovative therapeutics. [ABSTRACT FROM AUTHOR]

World Health Organisation recommends the practice of BCG vaccination at birth in countries which have a high incidence of tuberculosis and/or high leprosy burden. The BCG vaccination is considered safe for a competent immune system. However, in children with weakened immune systems cause of which can be primary or secondary, the vaccine may lead to side effects which can be localized or disseminated. In this study, we report a spectrum of inborn errors of immunity (IEI) commonly referred to as primary immunodeficiency disorders (PIDs) diagnosed in a large cohort of patients presenting with complications to BCG vaccination from India. Retrospective data analysis of patients referred to ICMR‐ National Institute of Immunohematology (ICMR‐NIIH) for IEI workup between 2007 and 2019 was done. IEI was identified in n = 52/90 (57.7%) patients presenting with BCG complications. Of these, n = 13(14.4%) patients were diagnosed with severe combined immune deficiency, n = 15(16.7%) with chronic granulomatous disease, n = 19(21.1%) with Inborn errors of IFN‐γ immunity, n = 4(4.4%) with Combined immunodeficiency and n = 1(1.1%) with Leucocyte Adhesion Deficiency type1. Majority of cases with BCGosis (88%) had an underlying IEI. This study strongly highlights the need for evaluation of patients with BCG complications for underlying IEI. While disseminated BCGosis strongly predicts underlying IEI, even localized persistent adenitis may be a warning sign of underlying IEI. It is also strongly recommended to record a family history of previous sibling death prior to administration of this live vaccine and deferring live vaccine till the diagnosis of IEI is ruled out in cases with a positive family history. [ABSTRACT FROM AUTHOR]

Summary: It is critically important for plants to control the trade‐off between normal growth and pathogen immunity. However, the underlying molecular mechanism remains largely unknown. Here we report such a mechanism controlled by WRKY70 and its partner CHYR1 in Arabidopsis.We found that both levels of the WRKY70 target gene SARD1 and the phosphorylated forms of WRKY70 were increased in WRKY70OE plants upon Pst DC3000 infection. Mechanistically, phosphorylation of WRKY70 at Thr22 and Ser34 occurs, which then activates SARD1 expression through binding to a WT box.Phosphorylated WRKY70 is degraded by 26S proteasome via CHYR1 when resuming normal growth after infection. In addition, nonphosphorylated WRKY70 represses SARD1 expression by binding to both W (inhibitory activity site) and WT (active activity site) boxes.The binding of WRKY70 to alternative cis‐elements of SARD1 through a phosphorylation‐mediated switch controlled by CHYR1 contributes to modulating the balance between immunity and growth. [ABSTRACT FROM AUTHOR]

Human platelets play important roles in several physiologic and pathologic processes. Platelet concentrates are activated with thrombin or calcium, resulting in a viscous coagulum (platelet gel [PG]), composed of 95% platelets at least. PG is increasingly used for the treatment of a variety of soft and hard tissue defects, most notably in the management of chronic non‐healing wounds. During wound healing, platelets not only play a critical role in primary hemostasis and thrombosis, but also release growth factors and cytokines to promote tissue regeneration, enhance collagen synthesis, and trigger an immune response. This review addresses a variety of aspects relevant to the functions of well‐known platelet growth factors, animal and clinical studies of PG in the last decade, and different sources of platelets for PG. PG is used for non‐healing chronic wounds, such as oral ulcerations related to epidermolysis bullosa and chronic graft‐versus‐host disease, for those, the traditional treatment effect is poor. PG maybe provide a new therapeutic direction for these diseases. Nevertheless, some uncertainty is present, the number of clinical studies is not enough. Hence, randomized controlled trials are still required to study the potential of the use of PG in the near future. [ABSTRACT FROM AUTHOR]

Podosphaera xanthii is the main causal agent of cucurbit powdery mildew and a limiting factor of crop productivity. The lifestyle of this fungus is determined by the development of specialized parasitic structures inside epidermal cells, termed haustoria, that are responsible for the acquisition of nutrients and the release of effectors. A typical function of fungal effectors is the manipulation of host immunity, for example the suppression of pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI). Chitin is a major component of fungal cell walls, and chitin oligosaccharides are well‐known PAMP elicitors. In this work, we examined the role of PHEC27213, the most highly expressed, haustorium‐specific effector candidate of P. xanthii. According to different computational predictions, the protein folding of PHEC27213 was similar to that of lytic polysaccharide monooxygenases (LPMOs) and included a conserved histidine brace; however, PHEC27213 had low sequence similarity with LPMO proteins and displayed a putative chitin‐binding domain that was different from the canonical carbohydrate‐binding module. Binding and enzymatic assays demonstrated that PHEC27213 was able to bind and catalyse colloidal chitin, as well as chitooligosaccharides, acting as an LPMO. Furthermore, RNAi silencing experiments showed the potential of this protein to prevent the activation of chitin‐triggered immunity. Moreover, proteins with similar features were found in other haustorium‐forming fungal pathogens. Our results suggest that this protein is a new fungal LPMO that catalyses chitooligosaccharides, thus contributing to the suppression of plant immunity during haustorium development. To our knowledge, this is the first mechanism identified in the haustorium to suppress chitin signalling. [ABSTRACT FROM AUTHOR]

Humans are exposed to varying amounts of ultraviolet radiation (UVR) through sunlight. UVR penetrates into human skin leading to release of neuropeptides, neurotransmitters and neuroendocrine hormones. These messengers released from local sensory nerves, keratinocytes, Langerhans cells (LCs), mast cells, melanocytes and endothelial cells (ECs) modulate local and systemic immune responses, mediate inflammation and promote differing cell biologic effects. In this review, we will focus on both animal and human studies that elucidate the roles of calcitonin gene‐related peptide (CGRP), substance P (SP), nerve growth factor (NGF), nitric oxide and proopiomelanocortin (POMC) derivatives in mediating immune and inflammatory effects of exposure to UVR as well as other cell biologic effects of UVR exposure. [ABSTRACT FROM AUTHOR]

Contaminants such as mercury are pervasive and can have immunosuppressive effects on wildlife. Impaired immunity could be important for forecasting pathogen spillover, as many land‐use changes that generate mercury contamination also bring wildlife into close contact with humans and domestic animals. However, the interactions among contaminants, immunity and infection are difficult to study in natural systems, and empirical tests of possible directional relationships remain rare.We capitalized on extreme mercury variation in a diverse bat community in Belize to test association among contaminants, immunity and infection. By comparing a previous dataset of bats sampled in 2014 with new data from 2017, representing a period of rapid agricultural land conversion, we first confirmed bat species more reliant on aquatic prey had higher fur mercury. Bats in the agricultural habitat also had higher mercury in recent years. We then tested covariation between mercury and cellular immunity and determined if such relationships mediated associations between mercury and bacterial pathogens. As bat ecology can dictate exposure to mercury and pathogens, we also assessed species‐specific patterns in mercury–infection relationships.Across the bat community, individuals with higher mercury had fewer neutrophils but not lymphocytes, suggesting stronger associations with innate immunity. However, the odds of infection for haemoplasmas and Bartonella spp. were generally lowest in bats with high mercury, and relationships between mercury and immunity did not mediate infection patterns. Mercury also showed species‐ and clade‐specific relationships with infection, being associated with especially low odds for haemoplasmas in Pteronotus mesoamericanus and Dermanura phaeotis. For Bartonella spp., mercury was associated with particularly low odds of infection in the genus Pteronotus but high odds in the subfamily Stenodermatinae.Synthesis and application. Lower general infection risk in bats with high mercury despite weaker innate defense suggests contaminant‐driven loss of pathogen habitat (i.e. anemia) or vector mortality as possible causes. Greater attention to these potential pathways could help disentangle relationships among contaminants, immunity and infection in anthropogenic habitats and help forecast disease risks. Our results also suggest that contaminants may increase infection risk in some taxa but not others, emphasizing the importance of considering surveillance and management at different phylogenetic scales. [ABSTRACT FROM AUTHOR]

The fetal inflammatory response (FIR) increases the risk of perinatal brain injury, particularly in extremely low gestational age newborns (ELGANs, < 28 weeks of gestation). One of the mechanisms contributing to such a risk is a postnatal intermittent or sustained systemic inflammation (ISSI) following FIR. The link between prenatal and postnatal systemic inflammation is supported by the presence of well‐established inflammatory biomarkers in the umbilical cord and peripheral blood. However, the extent of molecular changes contributing to this association is unknown. Using RNA sequencing and mass spectrometry proteomics, we profiled the transcriptome and proteome of archived neonatal dried blood spot (DBS) specimens from 21 ELGANs. Comparing FIR‐affected and unaffected ELGANs, we identified 782 gene and 27 protein expression changes of 50% magnitude or more, and an experiment‐wide significance level below 5% false discovery rate. These expression changes confirm the robust postnatal activation of the innate immune system in FIR‐affected ELGANs and reveal for the first time an impairment of their adaptive immunity. In turn, the altered pathways provide clues about the molecular mechanisms triggering ISSI after FIR, and the onset of perinatal brain injury. Databases: EGAS00001003635 (EGA); PXD011626 (PRIDE). [ABSTRACT FROM AUTHOR]

Temperate bacteriophages can display in a stable way two essentially different behaviours. In the immune state, a gene (cI) produces a repressor which prevents expression of all the other viral genes; in the non-immune state the typically viral functions are expressed. The choice between the two pathways and the establishment of one of them have much in common with cell determination and differentiation. This choice depends on a complex control system, in fact one of the most intricate nets of regulation known in some detail. Our paper provides a formal description and partial analysis of this regulatory net. It is shown that even for relatively simple known models, this kind of analysis uncovers predictions which had previously remained hidden. Some of these predictions were checked experimentally. The experimental part chiefly deals with the efficiency of lysogenization by thermoinducible lambda phage carrying mutations in one or more of the regulatory genes, N, cro and cII. Although N- mutations are widely known for preventing efficient integration, and both N- and cII mutations for preventing efficient establishment of immunity, it is shown that, as predicted by a simple model, both N- and cII- phage efficiently lysogenize at low temperature if they are in addition cro-. In contrast with lambda N- cro+, λ N- cro- is not propagated as a plasmid at low temperature, precisely because it establishes immunity too efficiently. Genetic control circuits are described in terms of sets of logic equations, which relate the state of expression of genes or of chemical reactions (functions) to input (genetic and environmental) variables and to the presence of gene and reaction products (internal, or memorization varibles). From the set of equations, one derives a matrix which shows the stable stationary states (if any) of the system, and from which one can derive the pathways (temporal sequences of states) consistent with the model. This kind of analysis is complementary to the more widely used analysis based on differential equations; it allows one to analyze in less detail more complex systems. The language might be used as well, mutatis mutandis, in fields very different from genetics. The last part of the discussion deals with the role of positive feedback loops in our specific problem (establishment and maintenance of immunity in temperate bacteriophages) and in developmental genetics in general. As a generalization of an old idea, it is suggested that cell determination (for a given character) depends on a set of genes whose interaction constitutes a positive feedback loop. Such a system has two stable stationary states: which one is chosen will usually depend on additional controls grafted on the loop. [ABSTRACT FROM AUTHOR]

This paper discusses noise immunity learning in speech recognition by word-spotting. In the proposed method, the learning speech data with superposed noise is constructed by adding the noise data to the clean speech data collected beforehand. Then the recognition dictionary for word-spotting is trained to improve noise immunity. In the learning, the recognition by word-spot- ting is attempted for the artificially synthesized learning data while gradually increasing the ratio of the contained noise. The recognition is executed using the learning word feature vector automatically extracted based on the similarity. The noise immunity is realized by the simulation in the noisy environment and the automatic learning. The recognition and learning use the word as the unit and the multiple similarity method, which can cope with a wide range of pattern deformation. An evaluation experiment is executed using 13-word speech data (plus noise in a railway station). For the case of 96-dimensional word feature vector (eight dimensions for frequency and 12 dimensions for time), and S/N ratio of 10 dB, the recognition rate is improved from 85.5 percent in the word-spotting method without laming to 94.1 percent with learning. This indicates the usefulness of the proposed method. [ABSTRACT FROM AUTHOR]

In 1941, techniques using fluorescent antibodies to locate antigens were used for the first time by Coons, Crech and Jones. Intercellular and epithelial antibodies in pemphigus vulgaris were demonstrated initially by Beutner and Jordan in 1964. The relationship between clinical severity and titers of serum antibodies has been a controversial subject. Antibodies are located in the intercellular spaces of the epidermis, where intraepidermal bullae with acantholytic cells develop. The antibodies are specific and present in almost all patients with active Brazilian pemphigus foliaceus.

PMN migration into the gingival sulcus is a tightly regulated process aimed at selectively increasing leukocyte availability at the site of bacterial plaque aggression, i.e. the superficial portion of the junctional epithelium. The evidence reviewed in this paper indicates that, besides the action of complement fragments, arachidonic acid metabolites, formyl peptides and other bacterial products, the establishment of a gradient of ICAM-1 expression across the junctional epithelium and the expression of IL-8 in its superficial layers probably represent important regulatory mechanisms leading to PMN migration into the gingival sulcus. Such mechanisms can be regulated by the autocrine and paracrine action of some pro-inflammatory cytokines and could possibly be initiated by specific bacteria-keratinocyte interactions. The advantage of such a redundant regulatory mechanism leading to PMN transepithelial migration is probably related to the key role of the neutrophil in the maintenance of a local host-parasite equilibrium on one side, and on the tissue injury associated with PMN persistence or random migration within periodontal tissues on the other. Several investigations are in progress aimed at identifying the initial environmental stimuli leading to PMN recruitment into the gingival sulcus and at further exploring the important regulatory events. [ABSTRACT FROM AUTHOR]

The principal aim of this work was to analyze the host systemic immune response to an oral infection of A. viscosus T14V. Previous work had established a Balb/c mouse model for A. viscosus T14V oral infection. Animals were infected and the splenocyte response to A. viscosus T14V antigens, LPS, and Con A were assessed in the lymphoblast assay. Splenocytes from mice infected with A. viscosus T14V exhibited an altered response pattern to the antigens and mitogens. The responses were enhanced or suppressed when compared to the uninfected control splenocyte response. The effluent cells from a nylon wool column were unresponsive to A. viscosus antigens but LPS did respond to Con A. This response pattern was true for splenocytes from infected and uninfected animals. These results suggest that A. viscosus T14V is a potent immunomodulater when analyzed within the BaIb/c mouse model system. [ABSTRACT FROM AUTHOR]

We have examined psychosocial and immune system stress responses in gay men before and after their notification of human immunodeficiency virus (HIV-1) status and as a consequence of stress management intervention procedures. Prior to notification, early stage, asymptomatic, seropositive men displayed compromised immunity as evidenced by significant decreases in CD4+ cell number, the helper subset (CD29+CD4+), CD4+/CD8+ ratio, and lymphocyte responses to mitogens. Prior to diagnosis, both seronegative and seropositive men revealed suppression of NK cell cytotoxicity and mitogen responsivity relative to matched laboratory control subjects not awaiting diagnosis. Immune suppression in these seronegative men disappeared after diagnosis, indicating its relationship to anticipation of serostatus notification. We also found that a 10-week program of aerobic exercise or psychosocial stress management buffered the psychological impact of notification of seropositivity. The aerobic exercise program produced a significant increase in CD+ and NKH.I + for seronegatives and CD45R + CD4+ cell number and mitogen responsivity for seropositives. We are assessing our interventions as tools for retarding immune deterioration and disease progression in HIV-1 seropositive individuals. [ABSTRACT FROM AUTHOR]

The immune system is usually viewed as an effector mechanism reacting to environmental antigenic challenge with defensive responses designed to eliminate 'foreign' substances and return to standby or surveillance mode. However, there is now substantial evidence to suggest that immunity is not effector-biased but is also a sensory organ and forms part of an integrated homeostatic network. Evidence that communication pathways exist between the immune and central nervous sytems which support bi-directional information flow, and that the output of the immune system influences other physiological adjustments to environmental change, is discussed in this paper, The proposition that an endocrine-immune gradient determines the homeostatic response to combined microbial and other ambient stressors is established and the potential for management of this gradient is explored. [ABSTRACT FROM AUTHOR]

Co-selection is a term used to denote the mutual positive selection of individual members from within two diverse populations, such that selection of members within one population is dependent on interaction with (recognition of) one or more member(s) within the other population. Coselection is a recurring theme of the idiotypic network model that my colleagues and I have developed. This paper discusses the role that co-selection plays in basic symmetrical network theory and in a network model that resolves the I-J paradox. It proposes that co-selection of helper T cells and HIV variants plays a role in the pathogenesis of AIDS. The AIDS model involves a role for the T cell receptor in the infection of T cells. Finally, a way in which a co-selection process may potentially be used in the prevention and therapy of harmful forms of immunity is described. [ABSTRACT FROM AUTHOR]

This paper presents an overview of the evolution of defence reactions in multicellular animal life. The co-evolution of hosts and pathogens provides the context to describe the major features of defence reactions and the countermeasures they evoke in their targets. Three major types of solutions to the riddle of self-non-self discrimination are discussed briefly: non-clonal recognition mediated by lectins, the preferential accumulation of C3 in microbial surfaces and vertebrate clonal immunity. Vertebrate immunity is described as a specialized type of inflammation against infectious agents that evolved in response to countermeasures successfully used by intracellular pathogens against non-specific defences. [ABSTRACT FROM AUTHOR]

Intrasplenic immunization with antigen immobilized on nitrocellulose (NC) paper results in an immune response with nanogram amounts of antigen without the use of Freund's adjuvant. Comparing the sensitivity of the intrasplenic immunization with intraperitoneal or subcutaneous administration, we found that the intrasplenic method resulted in more positive animals with higher titres than did the other techniques with the smallest amount of antigen (70 ng of bovine serum albumin). With larger amounts of albumin the intraperitoneal method yielded the highest titres. No loss of antigenicity was observed when we immunized with equal amounts of protein separated by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE), immunoblotted and stained with either Coomassie brilliant blue R 250 or Amido black 10 B. [ABSTRACT FROM AUTHOR]

The article discusses ligands and receptors in autoimmune systems. Brief information regarding ligands and receptors; Theories of idiotype network; Lists of diseases that involves autoimmunity to receptors; Utilization of the cellular receptor repertoire.

Delayed footpad reaction against syngeneic testicular cells was compared between males and virgin females of C3H/He mice. Mice were immunized subcutaneously with 1 × 107 of syngeneic testicular cells and the reaction was elicited with 1 × 106 of syngeneic testicular cells 6 days after the immunization. When mice were pretreated with 0, 25 or 50 mg/kg of cyclophosphamide (CY), the delayed footpad reaction was detected in female mice, but not in male mice under the same conditions. This sex difference in the reaction to testicular cells was not attributed to the recognition of H-Y antigen by female mice. A sex difference in the reaction to sheep red blood cells (SRBC) was not observed. The sex difference in the reaction to testicular cells was attributed to testicular cells other than sperm because a sex difference was not detected against sperm. The implications of these findings are discussed in relation to the tolerance phenomena of autologous testicular cells. [ABSTRACT FROM AUTHOR]

The effects of propamidine and their dose dependency, on utilization of the third and fifth complement components in immune haemolysis have been compared. While C3 utilization is not disturbed that of CS is markedly inhibited by propamidine in concentrations as low as 0.5 mist Both, binding of CS to surface-fixed C3b and cleavage of CS by convertases C42 and C3bBb, are also inhibited in the presence of propamidine. Since neither C3 cleavage by these enzymes nor even C5 cleavage by the cobra venom factor-supported convertase CFVBb is significantly reduced a general convertase-inhibiting effect of propamidine is ruled out. Rather the effect on utilization of C5 is the result of interference with binding of CS to C3b and hence impairment of its accessibility to the convertases. These findings thus further support the role of surface-fixed C3b in C5 activation proposed earlier. [ABSTRACT FROM AUTHOR]

Anti-picrylsuppressor factor was prepared in the standard way, i.e. by culturing lymphoid cells from mice injected with picrysulphonic acid and then painted with picryl chloride and taking the supernatant fluid. It was assessed by its ability to depress the passive transfer of contact sensitivity by immune cells incubated in it. The factor can be specifically absorbed by picryl (but not oxazolone) albumin sepharose beads and can be specifically eluted by picryl (but not oxazolone) ϵ-aminocaproic acid and by picryl-ϵ-N-lysine. These findings emphasise the role of the hapten epitope in the binding of a specific T cell product. The factor can also be absorbed by Concanavalin A sepharose and can be eluted by an appropriate sugar such as ɑ-methylmannoside, but not by an inappropriate sugar such as lactose. It was possible to undertake two sequential affinity chromatography steps—first absorption with picryl albumin sepharose and elution with picryl-ϵ-N-lysine followed immediately by absorption by Con A sepharose and elution with α-methylmannoside. The availability of sequential affinity chromatography provides a simple approach to the purification of specific T suppressor factor. [ABSTRACT FROM AUTHOR]

Lymph node cells from immunized rabbits were cultured with varying concentrations of antigen in preheated (56°, 30 minutes) autologous serum which had been collected before immunization. [3H]Thymidine was present for the last 6 hours of the 24-hour culture period and the radioactive labelling of acid-precipitable material was then determined. Changes in labelling due to variations of culture conditions were interpreted according to whether they were specific for control or antigen-treated cultures or non-specific. Cell concentration and serum concentration were predominantly non-specific variables influencing the labelling in control and antigen-treated cultures to a proportionate extent. However, at serum concentrations below 5 per cent labelling was disproportionately inhibited in antigen-treated cultures; there were further minor disproportionate inhibitions at higher serum concentrations. Labelling was inhibited by increasing the concentration of serum from 25 to 50 per cent, mainly due to a non-diffusible competitive inhibitory activity. Isotope-dilution analysis of the effects of serum on labelling over a wide range of serum concentrations indicated that the relationship was a complex one with at least three step-wise stimulations of the maximum labelling rate being produced by increasing the serum concentrations from 0 to 25 per cent. Labelling in antigentreated cultures containing post-immunization serum was less than labelling in cultures containing an equal volume of preimmunization serum, but labelling in control cultures was enhanced by post-immunization serum. These results are shown to be compatible with the proposals (i) that labelling in control cultures reflects the response of cells to low concentrations of endogenous antigens, and (ii) that preimmunization serum and post-immunization serum contain ‘natural’ and ‘acquired’ antibodies respectively, which normally buffer cell-borne receptor sites against reaction with endogenous and exogenous antigens. [ABSTRACT FROM AUTHOR]

Serum protein, immunoglobulins, complement, lysozyme, serum bactericidal activity and blast transformation of peripheral blood lymphocytes were tested in beef cattle in different herds and age groups. These parameters were evaluated in their time-kinetics, in comparison with age-matched groups of dairy cattle. Like dairy calves, beef calves up to 4 months of age were shown to have low levels of serum bactericidal activity and haemolytic complement; besides, a worse profile was detected in serum protein and γ 2 globulin levels. Al(OH)3 and oil-adjuvanted vaccines had a favourable influence on immunoglobulin and lysozyme synthesis. An acute stressing event like transportation was shown to decrease mitogen-driven lymphocyte stimulation for at least 10 days after arrival. Zusammenfassung Untersuchung einiger Parameter der unspezifischen Infektabwehr beim Fleischrind In verschiedenen Mastbetrieben wurde von Tieren unterschiedlichen Alters Serumprotein- und Immunglobulingehalt, Komplement, Lysozym und die bakterizide Wirkung des Serums untersucht. Weiterhin wurde die Blasten transformierende Wirkung peripherer Blutlymphozyten bestimmt. Diese Parameter wurden über einen längeren Zeitraum gemessen und mit Werten von gleichaltrigen Milchviehkälbern verglichen. Bis zum Alter von 4 Monaten war in beiden Gruppen die bakterizide Wirkung und der Gehalt an Komplement gering, allerdings wiesen die Kälber der Fleischrassen niedrigere Serumprotein- und γ 2 Globulinwerte auf. Eine Immunisierung mit Al(OH)3 und öligem Adjuvans stimulierte die Immunglobulin- und Lysozymsynthese. Durch Transportstreß war die mitogen induzierte Lymphozytenstimulation für wenigstens 10 Tage nach Ankunft der Tiere reduziert. [ABSTRACT FROM AUTHOR]

Primed LD typing cells were prepared against single HLA baplotypes within families and used to type a random panel of 48 individuals. PLT cells could be grouped on the basis of highly correlated responses with the panel test cells; the 21 different PLT cells could be used to define 6 different PL antigens. One of these, PL 3, was split by the responses of two of the 21 PLT cells which measured an antigen called PL 3.1. [ABSTRACT FROM AUTHOR]

Four allergologically important fungi, viz. Aspergillus fumigatus, Penicillium notalum Alternaria altermata, and Cladosporium herbarum were cultured in a liquid synthetic me with or without addition of 0.1 % yeast extract (YE). After 10 and 28 days of cultivation, immunochemical properties of the fungal extracts, characterised by precipitation pattern and IgG- and IgE-binding capacity, were studied. In pure synthetic medium no large differences were observed in number of precipitates, as measured by DID, among the four antigenic fractions of each fungus (metabolic and mycelial antigens of both early and late phase cultures). Addition of YE to the growth medium hardly changed the number of precipitates and generally caused a decrease in lgG-binding capacity of the extracts. In contrast to these observations were the findings with the IgE-binding capacities of the fungal extracts as measured by RAST. Most allergenic fractions demonstrated an increase (sometimes strong) in lgE-binding capacity after YE was added to the growth medium. It is concluded that the time of cultivation influences the immunochemical characteristics of fungal extracts and that mycelial as well as metabolic antigens of both early and late phase cultures should be used in order to obtain a wide spectrum of allergens in extracts used for diagnostic purposes. [ABSTRACT FROM AUTHOR]

IgE and IgG antibodies (ab) and lymphocyte transformation (LT) were studied in untreated and hyposensitized birch pollen allergic subjects and in non-a topic controls using whole extract and fractions obtained by gel filtration of birch pollen extract. All the allergic subjects had positive IgE ab, IgG ab and LT responses to the whole extract. Both the untreated and the hyposensitized subjects had peak IgE ab and LT responses against the allergenic fractions of the extract, while negative responses were obtained in the non-atopic controls. Only hyposensitized subjects had developed high IgG ab responses to the allergenic fractions. Most of the treated and untreated subjects showed IgG ab and LT responses to the high molecular weight fractions with low allergenic activity. Significantly higher IgE ab responses to these fractions were observed in the treated subjects than in the untreated ones, indicating potentiation of IgE ab responses against some antigens during immunotherapy. Some of the allergic subjects also responded to the fractions of low molecular size (mol.wt. 2000-5000) with low allergenic activity. Both IgE ab, IgG ab and LT responses to these fractions were observed. [ABSTRACT FROM AUTHOR]

The article presents abstracts of several research papers published in different journals. One of the abstracts is on quantitative studies describing the in vivo behavior of an inhaled protein antigen. Aerosol mists were generated from bovine serum albumin (BSA) solutions. The fate of inhaled BSA in vivo was studied in rabbits by using a paired-isotope technique to quantitative antigen sequestration within organs. The study suggests that antigen inhalation may function primarily as an important physiologic means by which natural immunity to environmental antigens is established. Another abstract discusses relationship of serum theophylline concentration to inhibition of exercise-induced bronchospasm and comparison with cromolyn. The effect of cromolyn in suppressing exercise-induced bronchospasm was generally much less.

Satellite bacteriophage P4 immunity is encoded within a short DNA region 357 bp long containing the promoter PLE and 275 bp downstream. PLE is active both in the early post-infection phase, when genes necessary for P4 lytic cycle are transcribed from this promoter, and in the lysogenic condition, when expression of the above genes is prevented by prophage immunity. In order to understand how P4 immunity is elicited, we have characterized the transcription pattern during the establishment and the maintenance of the satellite phage P4 lysogenic condition. We found that prophage transcription starting at PLE ends prematurely and the transcripts do not extend beyond 300-400 nucleotides downstream of PLE. Thus P4 immunity acts by causing premature transcription termination rather than by repressing transcription initiation. The P4 immunity region is transcribed in the prophage, but it does not seem to be translated; this region contains two elements (seqA and seqB) of a palindromic sequence. In addition to transcripts about 300 nucleotides long, P4 prophage produces a family of shorter transcripts, about 80 nucleotides long, containing seqA or seqB. Evidence is presented suggesting that SeqB RNA is the transacting immunity factor, and that interaction of SeqB RNA with the complementary nascent RNA containing seqA may be involved in bringing about premature transcription termination. [ABSTRACT FROM AUTHOR]