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The Arctic region's unfavorable living conditions adversely affect the spread of infectious diseases, including COVID-19, This, in turn, can also lead to increased morbidity and mortality rates in the area due to a number of factors such as climate, environment, and high prevalence rate of pre-existing health issues like diabetes, obesity, and respiratory infections. These circumstances adversely affect maintaining the level of working capability. The aim of this paper is to investigate the ratio of immunocompetent cells involved in the adaptive post-COVID-19 immune response. The research includes an immunological assessment of 29 women aged 20-40 years residing in Arkhangelsk, Russia, six months after recovering from COVID-19. The count of leukocytes in the peripheral blood and their differ ential were evaluated using standard methods to assess the immunological status. To delve deeper into the immunological landscape, phenotypes of lymphocytes (CD5+, CD8+, CD10+, and CD95+) were evaluated using an indirect immunoperoxidase reaction with monoclonal antibodies on dried drop lymphocyte preparations. After incubating blood with latex molecules, the activity and quantity of phagocytes were assessed using a light microscope. The neutrophil/lymphocyte ratio was found to be inverted in the female subjects under investigation. The high concentration of cytotoxic T-lymphocytes (CD8+) and lymphocytes with apoptotic receptors (CD95+) suggests a potential correlation with a concurrent reduction in the expression of the total T-cell marker (CD5+) across all cases. This association was further linked to a decrease in lymphoproliferative activity and a relative decline in phagocytic activity. These findings led us to posit that the total recovery time after COVID-19 might extend beyond six months, indicative of a prolonged impact on the body's protective capacity. Our observations prompt the hypothesis that cellular immunity plays a crucial role in determining the severity of COVID-19 infection. Specifically, individuals with initially robust phagocytic activity may be predisposed to experiencing a milder form of the infection. However, this assumption warrants further investigation and clarification in individuals with moderate and severe disease progression [ABSTRACT FROM AUTHOR]

This paper aims to compare the cellular immune response to the SARS-CoV-2 BNT162b2 vaccine of pediatric patients with autoimmune inflammatory rheumatic disease (pAIIRD) and healthy controls. A prospective longitudinal study was conducted between April 2021 and December 2022 at the Tel Aviv Medical Center. Children <18 years, with pediatric-onset AIIRD and healthy controls, who have received at least two doses of the BNT162b2 vaccine, were included. Humoral response was evaluated by serum levels of anti-SARS-CoV-2 receptor-binding domain antibodies. Cellular response was evaluated by flow cytometry, measuring IFNγ and TNFα production by CD4+ T cells following stimulation with SARS-CoV-2 Spike peptide mix. The study included 20 pAIIRD patients and 11 controls. The mean age of participants was 12.6 ± 2.94 years, with 58.1% females. The cellular response to the BNT162b2 vaccine was statistically similar in both groups. However, the humoral response was statistically lower in pAIIRD compared with the healthy control group. There was no statistically significant correlation between the humoral response and cellular response. During the study period, 43.75% of AIIRD children and 72.7% of controls had a breakthrough COVID-19 infection (P = 0.48). Bivariate models examining the effect of the cellular response and presence of an AIIRD on breakthrough infections found no effect. Compared with healthy controls, pAIIRD demonstrated similar cellular responses. Patients showed reduced humoral response compared with healthy adolescents, but similar breakthrough infection rates. These findings may support the importance of the cellular response in protecting against COVID-19 infections. Pediatric rheumatic patients may be vulnerable to COVID-19 infections due to their disease and immunosuppressive medications. Compared with healthy controls, pediatric patients with autoimmune inflammatory rheumatic diseases demonstrated similar cellular responses and COVID-19 breakthrough infection rates, but reduced humoral responses. These findings may support the importance of the cellular response in protecting against COVID-19 infections. Graphical Abstract [ABSTRACT FROM AUTHOR]

This article follows-up on our recently published work, which evaluated the impact of the addition of an alfalfa leaf-derived adsorbent in the aflatoxin B1 (AFB1)-contaminated diet in regard to the production parameters, blood cell count, serum biochemistry, liver enzymes, and liver histology of turkey poults. This paper presents complementary results on microbial community, ileal morphology, barrier function, and immunity. For this purpose, 350 1-day-old female turkey poults were randomly distributed into five groups: (1) Control, AFB1-free diet; (2) AF, AFB1-contaminated diet at 250 ng/g; (3) alfalfa, AFB1-free diet + 0.5% (w/w) adsorbent; (4) alfalfa + AF, AFB1-contaminated diet at 250 ng/g + 0.5% (w/w) adsorbent; and (5) YCW + AF, AFB1-contaminated diet at 250 ng/g + 0.5% (w/w) commercial yeast cell wall-based adsorbent (reference group). In general, in the AF group, the growth of opportunistic pathogens was promoted, which lead to gut dysbacteriosis, mainly influenced by Streptococcus lutetiensis. Conversely, a significant increase in beneficial bacteria (Faecalibacterium and Coprococcus catus) was promoted by the addition of the plant-based adsorbent. Moreover, the AF group had the lowest villus height and a compromised barrier function, as evidenced by a significant (p < 0.05) increase in fluorescein isothiocyanate dextran (FITC-d), but these negative effects were almost reversed by the addition of the alfalfa adsorbent. Furthermore, the AF + YCW and alfalfa + AF groups exhibited a significant increase in the cutaneous basophil hypersensitivity response compared to the rest of the experimental groups. Taken together, these results pointed out that the alfalfa counteracts the adverse effects of AFB1 in poults, facilitating the colonization of beneficial bacteria and improving the barrier function of the turkey poults. [ABSTRACT FROM AUTHOR]

In the last few years, a lot of publications suggested that disabling cerebellar ataxias may develop through immune-mediated mechanisms. In this consensus paper, we discuss the clinical features of the main described immune-mediated cerebellar ataxias and address their presumed pathogenesis. Immune-mediated cerebellar ataxias include cerebellar ataxia associated with anti-GAD antibodies, the cerebellar type of Hashimoto's encephalopathy, primary autoimmune cerebellar ataxia, gluten ataxia, Miller Fisher syndrome, ataxia associated with systemic lupus erythematosus, and paraneoplastic cerebellar degeneration. Humoral mechanisms, cell-mediated immunity, inflammation, and vascular injuries contribute to the cerebellar deficits in immune-mediated cerebellar ataxias. [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]

The CD58-CD2 axis regulates T cell-mediated cancer immunity, but little is known about the regulation of CD58. In two recent papers pubished in Cancer Cell , Miao et al. and Ho et al. define a mechanism of CD58 regulation by CMTM6 and show an unexpected yin-yang link between PD-L1 and CD58. The CD58-CD2 axis regulates T cell-mediated cancer immunity, but little is known about the regulation of CD58. In two recent papers published in Cancer Cell , Miao et al. and Ho et al. define a mechanism of CD58 regulation by CMTM6 and show an unexpected yin-yang link between PD-L1 and CD58. [ABSTRACT FROM AUTHOR]

Recent events highlighted that, despite decades of studying vaccine immunogenicity and efforts toward finding correlates of protection, evaluating real-world vaccine efficacy as well as establishing meaningful licensing criteria still represents a significant challenge. In this paper, we review all aspects of influenza vaccine immunogenicity, including animal and human challenge studies, humoral and cellular immunity parameters, and their potential correlation with real-life protection from disease. [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]

Transferrin receptor 1 (TfR1) is a type II membrane protein that mediates cellular iron uptake. Transferrin receptor 2(TfR2), another receptor for transferrin (Tf), has recently been cloned. We examined expression levels of TfR1, TfR2-α (membrane form) and TfR2-β (non-membrane form) transcripts in cells from 67 patients with de novo acute myeloid leukaemia (AML) using reverse transcription-polymerase chain reaction (RT-PCR), and correlated the results with a variety of clinical features and disease outcomes of these patients. Significant correlations were noted between the levels of both TfR1 and TfR2-α ( r = 0·771, P < 0·001) and TfR1 and TfR2-β ( r = 0·534, P < 0·001). Unexpectedly, initial white blood cell (WBC) counts were inversely correlated with levels of expression of either TfR1( r = −0·357, P = 0·003), TfR2-α ( r = −0·486, P < 0·0001), or TfR2-β ( r = −0·435, P = 0·0003). Only TfR2 expression was significantly associated with either serum iron ( r = −0·270, P = 0·045) or serum ferritin ( r = −0·364, P = 0·008). Multivariate analyses using Cox's proportional hazard model showed that elevated TfR2-α, but not TfR1 or TfR2-β mRNA levels significantly contributed to a better prognosis for AML patients. Furthermore, a group with high expression levels of both TfR2-α and TfR2-β survived significantly longer than a group without high expression of both of them ( P < 0·01 by log-rank). The present study suggests that (i) TfRs-independent iron uptake might have an important role in in vivo proliferation of AML cells; (ii) expression of TfR2 (especially the α form) is a novel prognostic factor for patients with AML. [ABSTRACT FROM AUTHOR]

Introduction: For patients with gastric cancer who have undergone gastrectomy, recent research has shown that enteral immunonutrition (EIN) is more successful than enteral nutrition (EN) at boosting host immunity and, in turn, improving prognosis. The claimed outcomes, however, are inconsistent. Aim: This meta-analysis examines how EIN affects biochemical, immunological, and clinical outcomes for gastrectomy (GC) patients following gastrectomy and EIN formulae evidence networks. Material and methods: A comprehensive search of the Medline, EMBASE, Scopus, and Cochrane Library databases identified English-language peer-reviewed journal papers. The odds ratio (OR) and standard mean difference (SMD) were calculated, along with their 95% confidence intervals. The heterogeneity was assessed using Cochrane Q and I2 statistics and the appropriate p-value. The analysis used RevMan 5.3. Results: This meta-analysis included 10 RCTs involving 1409 GC patients, 714 of whom were assigned to EIN and 695 to EN. After EIN treatment, serum proalbumin, serum transferrin, lymphocyte count, and CD4+/CD8+ ratio had statistically significant standardised mean differences (SMDs) of 2.39, 2.39, 1.34, and 0.72, respectively. EIN reduces postoperative infectious complications with an OR of 0.63 (95% CI: 0.41--0.77) for infections, an OR of 0.63 for complications, and an SMD of --1.05 for systemic inflammations. A network diagram with high-quality data and a well-defined network design with consistent and accurate connection shows that EIN can improve serum protein levels, immunological parameters, and post-operative problems. Conclusions: The use of EIN has been shown to enhance cellular immunity, regulate inflammatory response, and decrease postoperative complications in GC patients who underwent major GI surgery. [ABSTRACT FROM AUTHOR]

In this paper, we incorporate immune systems containing Cytotoxic T lymphocyte and humoral immunity into a general human immunodeficiency viruses infection model, which also considers logistic growth for target cells and both modes of spread, cell-to-cell and cell-free represents, by linear functions. We derive five threshold parameters which are used to study the existence of equilibria. By considering the characteristic equations, the local stability of disease-free and immune-free equilibria is investigated. Lyapunov functions and LaSalle's invariance are constructed to prove the global stability of all steady states. Global dynamics of the human immunodeficiency viruses model can be accurately expressed by threshold parameters; also the existence of Hopf bifurcation is discussed and the results are expressed in the form of a proposition. Furthermore, numerical simulations confirm the corresponding theoretical results. [ABSTRACT FROM AUTHOR]

Simple Summary: Natural killer cells are a part of the native immune response to cancer. NK cell-based immunotherapies are an emerging strategy to kill tumor cells. This paper reviews the role of NK cells, their mechanism of action for killing tumor cells, and the receptors which could serve as potential targets for signaling. In this review, the role of nanoparticles in NK cell activation and increased cytotoxicity of NK cells against cancer are highlighted. Natural killer (NK) cells are one of the first lines of defense against infections and malignancies. NK cell-based immunotherapies are emerging as an alternative to T cell-based immunotherapies. Preclinical and clinical studies of NK cell-based immunotherapies have given promising results in the past few decades for hematologic malignancies. Despite these achievements, NK cell-based immunotherapies have limitations, such as limited performance/low therapeutic efficiency in solid tumors, the short lifespan of NK cells, limited specificity of adoptive transfer and genetic modification, NK cell rejection by the patient's immune system, insignificant infiltration of NK cells into the tumor microenvironment (TME), and the expensive nature of the treatment. Nanotechnology could potentially assist with the activation, proliferation, near-real time imaging, and enhancement of NK cell cytotoxic activity by guiding their function, analyzing their performance in near-real time, and improving immunotherapeutic efficiency. This paper reviews the role of NK cells, their mechanism of action in killing tumor cells, and the receptors which could serve as potential targets for signaling. Specifically, we have reviewed five different areas of nanotechnology that could enhance immunotherapy efficiency: nanoparticle-assisted immunomodulation to enhance NK cell activity, nanoparticles enhancing homing of NK cells, nanoparticle delivery of RNAi to enhance NK cell activity, genetic modulation of NK cells based on nanoparticles, and nanoparticle activation of NKG2D, which is the master regulator of all NK cell responses. [ABSTRACT FROM AUTHOR]

Cellular immunity against SARS-CoV-2 is an important component of the immune response to the virus. At present, two such tests based on interferon-gamma release (interferon-γ release assays, IGRAs) are available—Quan-T-Cell SARS-CoV-2 by EUROIMMUN and T-SPOT.COVID by Oxford Immunotec. In this paper, we compared the results of these two tests in 90 subjects employed at the Public Health Institute Ostrava who had previously undergone COVID-19 infection or were vaccinated against that disease. To the best of our knowledge, this is the first head-to-head comparison of these two tests evaluating T-cell-mediated immunity against SARS-CoV-2. In addition, we also evaluated humoral immunity in the same individuals using the in-house virus neutralization test and IgG ELISA assay. The evaluation yielded similar results for both IGRAs, with Quan-T-Cell appearing to be insignificantly (p = 0.08) more sensitive (all 90 individuals were at least borderline positive) than T-SPOT.COVID (negative results found in five patients). The overall qualitative (presence/absence of immune response) agreement of both tests with virus neutralization test and anti-S IgG was also excellent (close or equal to 100% in all subgroups, with the exception of unvaccinated Omicron convalescents, a large proportion of whom, i.e., four out of six subjects, were IgG negative while at least borderline positive for T-cell-mediated immunity measured by Quan-T). This implies that the evaluation of T-cell-mediated immunity is a more sensitive indicator of immune response than the evaluation of IgG seropositivity. This is true at least for unvaccinated patients with a history of being infected only by the Omicron variant, but also likely for other groups of patients. [ABSTRACT FROM AUTHOR]

The SARS-CoV-2 pandemic has demonstrated the need to create highly effective antivirals and vaccines against various RNA viruses, including SARS coronaviruses. This paper provides a short review of innovative strategies in the development of antivirals and vaccines against SARS coronaviruses, with a focus on antisense antivirals, oligonucleotide adjuvants in vaccines, and oligonucleotide vaccines. Well-developed viral genomic databases create new opportunities for the development of innovative vaccines and antivirals using a post-genomic platform. The most effective vaccines against SARS coronaviruses are those able to form highly effective memory cells for both humoral and cellular immunity. The most effective antivirals need to efficiently stop viral replication without side effects. Oligonucleotide antivirals and vaccines can resist the rapidly changing genomic sequences of SARS coronaviruses using conserved regions of their genomes to generate a long-term immune response. Oligonucleotides have been used as excellent adjuvants for decades, and increasing data show that oligonucleotides could serve as antisense antivirals and antigens in vaccine formulations, becoming a prospective tool for immune system tuning. [ABSTRACT FROM AUTHOR]

The article presents abstracts from papers related to research on amino acids that were published in the February 2005 issue of the "Journal of Animal Science." The paper "Apparent and True Ileal Amino Acid and Energy Digestibility and Weanling Pig Performance of Five Sources of Distillers Dried Grains With Solubles," by N.D. Fastinger and D.C. Mahan, evaluated the apparent and true ileal amino acid digestibility of distillers dried grains with solubles from five plants. The paper "Effects of Orally Administered 25-Hydroxyvitamin D and Vitamin E on Calcium and Vitamin D Metabolites in Plasma and on Vitamin D Metabolites in Beef Longissimus Dorsi Muscle," was presented by K.M. Carnagey, A.E. Wertz, T.J. Knight, E.J. Huff-Lonergan, A.H. Trenkle and D.C. Beitz. The paper "Inflammatory Cytokines Differentially Modulate the Adiponectin Receptors 1 and 2 in Pig Subcutaneous Adipocytes," by S. Jacobi and M. Spurlock, indicated that pro-inflammatory cytokines act directly on adipocytes to down regulate adiponectin receptor expression.

Simple Summary: Cancer in the head and neck region (HNSCC) is exponentially increasing due to human papillomavirus (HPV) infections. This paper helps us to understand the complexity of the inflammatory networks and the mechanisms of immune evasion in HPV+ HNSCC to open up new avenues and drive the discovery of useful tools to be translated clinically in the screening and treatment of these cases, especially to overcome resistance and improve patients' quality of life. Head and neck squamous cell carcinomas (HNSCC) are a heterogeneous group of malignancies which have shown exponential incidence in the last two decades especially due to human papillomavirus (HPV) infection. The HPV family comprises more than 100 types of viruses with HPV16 and HPV18 being the most prevalent strains in HNSCC. Literature data reveal that the mutation profile as well as the response to chemotherapy and radiotherapy are distinct among HPV+ versus HPV-negative tumors. Furthermore, the presence of the virus induces activation of an immune response, in particular the recruitment of specific antiviral T lymphocytes to tumor sites. These T cells when activated produce soluble factors including cytokines and chemokines capable of modifying the local immune tumor microenvironment and impact on tumor response to the treatment. In this comprehensive review we investigated current knowledge on how the presence of an HPV can modify the inflammatory response systemically and within the tumor microenvironment's immunological responses, thereby impacting on disease prognosis and survival. We highlighted the research gaps and emerging approaches necessary to discover novel immunotherapeutic targets for HPV-associated HNSCC. [ABSTRACT FROM AUTHOR]

The immune response plays a crucial role in preventing diseases, such as infections. There are two types of immune responses, specific and innate immunity, each of which consists of two components: cellular immunity and humoral immunity. Dysfunction in any immune system component increases the risk of developing certain diseases. Systemic lupus erythematosus (SLE), an autoimmune disease in the human body, develops an immune response against its own components. In these patients, due to underlying immune system disorders and receipt of immunosuppressive drugs, the susceptibility to infections is higher than in the general population and is the single largest cause of mortality in this group. COVID-19 infection, which first appeared in late 2019, has caused several concerns in patients with SLE. However, there is no strong proof of additional risk of developing COVID-19 in patients with SLE, and in some cases, studies have shown less severity of the disease in these individuals. This review paper discusses the immune disorders in SLE and COVID-19. [ABSTRACT FROM AUTHOR]

Crustaceans such as shrimps and crabs, hold significant ecological significance and substantial economic value within marine ecosystems. However, their susceptibility to disease outbreaks and pathogenic infections has posed major challenges to production in recent decades. As invertebrate, crustaceans primarily rely on their innate immune system for defense, lacking the adaptive immune system found in vertebrates. Mucosal immunity, acting as the frontline defense against a myriad of pathogenic microorganisms, is a crucial aspect of their immune repertoire. This review synthesizes insights from comparative immunology, highlighting parallels between mucosal immunity in vertebrates and innate immune mechanisms in invertebrates. Despite lacking classical adaptive immunity, invertebrates, including crustaceans, exhibit immune memory and rely on inherent "innate immunity factors" to combat invading pathogens. Drawing on parallels from mammalian and piscine systems, this paper meticulously explores the complex role of mucosal immunity in regulating immune responses in crustaceans. Through the extrapolation from well-studied models like mammals and fish, this review infers the potential mechanisms of mucosal immunity in crustaceans and provides insights for research on mucosal immunity in crustaceans. • Mucosal immunity parallels cellular and humoral immunity and interacts closely with the lymphatic system. • Vertebrate mucosal immunity shows significant convergence with invertebrate innate immunity. • Mucosal immunity probably exists in crustaceans. [ABSTRACT FROM AUTHOR]

Tuberculosis (TB) is one of humanity's three major infectious diseases. Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia due to impaired insulin secretion or impaired insulin function. It has been reported that DM is a primary risk factor for TB disease. Given the increasing public health threat to people's health, more and more studies have focused on diabetes complicated by TB. Hyperglycemia can affect the function of human immune cells, promote primary infections and reactivation of TB, and increase the susceptibility and severity of TB. However, the immunological mechanism behind it is still not clear. By reviewing the related articles on tuberculosis complicated with diabetes published in recent years, this paper expounds on the effect of hyperglycemia on innate immunity and adaptive immunity of patients with TB. This review provides new insights for elucidating the immunological mechanism of TB complicated with DM and lays the foundation for finding potential targets for preventing and treating TB combined with DM. [ABSTRACT FROM AUTHOR]

The new COVID-19 variants are triggering a fresh panic all around. Scientists still have not found any closely related identification of these variants in the context of their evolution. The scrupulous deletion/mutations recognized inside the spike protein of the variants are emerging with an amplified pace and are observed to be associated with the alterations in the receptor-binding region (RBD) of the spike protein. This paper highlights the reported mechanistic studies conducted on SARS-CoV-2 mutant variants; the mutant virus's ability in response to the antibody recognition to evade the immune system in humans. The role of cellular immunity in response to its interaction with SARS-CoV-2 variants and importantly the discussion on the antibody-dependent enhancement (ADE) of SARS-CoV-2 disease with therapeutic antibodies and vaccines has been highlighted. It is expected that this may likely be interesting and helpful for readers in clearing all their presumptions related to the spreading severity of the mutant virus strains and more importantly the effectiveness of current and upcoming vaccines for its possible control. [ABSTRACT FROM AUTHOR]

[Display omitted] The recent ongoing outbreak of coronavirus disease 2019 (COVID-19), still is an unsolved problem with a growing rate of infected cases and mortality worldwide. The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is targeting the angiotensin-converting enzyme 2 (ACE2) receptor and mostly causes a respiratory illness. Although acquired and resistance immunity is one of the most important aspects of alleviating the trend of the current pandemic; however, there is still a big gap of knowledge regarding the infection process, immunopathogenesis, recovery, and reinfection. To answer the questions regarding "the potential and probability of reinfection in COVID-19 infected cases" or "the efficiency and duration of SARS-CoV-2 infection-induced immunity against reinfection" we critically evaluated the current reports on SARS-CoV-2 immunity and reinfection with special emphasis on comparative studies using animal models that generalize their finding about protection and reinfection. Also, the contribution of humoral immunity in the process of COVID-19 recovery and the role of ACE2 in virus infectivity and pathogenesis has been discussed. Furthermore, innate and cellular immunity and inflammatory responses in the disease and recovery conditions are reviewed and an overall outline of immunologic aspects of COVID-19 progression and recovery in three different stages are presented. Finally, we categorized the infected cases into four different groups based on the acquired immunity and the potential for reinfection. In this review paper, we proposed a new strategy to predict the potential of reinfection in each identified category. This classification may help to distribute resources more meticulously to determine: who needs to be serologically tested for SARS-CoV-2 neutralizing antibodies, what percentage of the population is immune to the virus, and who needs to be vaccinated. [ABSTRACT FROM AUTHOR]

The article provides information on pathogen Listeria monocytogenes. According to a research, such pathogen takes advantage of a facet of its host's immune response and it produces a protein called listeriolysin O (LLO) that injects pores into membranes. This action allows the bacterium to escape from intracellular areas charged with its destruction and to replicate and spread.

In this paper, we propose and investigate a fractional diffusive model for hepatitis B virus (HBV) infection with capsids and immune response presented by cytotoxic T lymphocyte (CTL) cells. We derive the conditions for global asymptotic stability of the steady states of the model in terms of the basic reproduction number R0 and the immune response reproduction number R1. By constructing appropriate Lyapunov functionals, it is shown that the infection-free equilibrium is globally asymptotically stable when R0 ≤ 1, the immune-free infection equilibrium is globally asymptotically stable when R1 ≤ 1 < R0 and the infection equilibrium with CTL immune response is globally asymptotically stable when R1 > 1. Numerical simulations are performed to illustrate the analytical results. [ABSTRACT FROM AUTHOR]

• We first described the S.maltophilia immunosuppressive effect on T cells and it is meaningful for immunosuppressed patients or co-infections. • T cells stimulated by S.maltophilia with CD4 and CD8 degraded via PD-1/PD-L1 pathway, which led to the massive apoptosis of T cells. • T cells were stimulated by S. maltophilia to secrete IFN-γ. Blocking the PD-1/PD-L1 pathway, apoptosis was suppressed. • S.maltophilia down-regulates host immunity by inhibiting immune cells. Smalotrophomonas maltophilia (S. maltophilia) is common in nosocomial infections. However, few studies have revealed the effect of S. maltophilia on cellular immunity in the host's immune system up to now. In clinical work, we accidentally discovered that S. maltophilia directly stimulated T cells to secrete IFN-γ. S. maltophilia was co-cultured with PBMCs to detect secretion of cytokines (IFN-γ, TNF-α and IL-2) and expression of cell surface molecules (CD3, CD4, CD8, CD69, CD147 and CD152) of T cells. We used light microscopy and electron microscopy to observe the cell morphology and subcellular structure of S. maltophilia co-cultured with lymphocytes. Flow cytometry and Western Blot were used to detect the expression of PD-1/PD-L1 and annexin V in cells. T cells stimulated by S. maltophilia secreted a large amount of IL-2, IFN-γ, and TNF-α. The expression of CD4 and CD8 on the cell surface were declined, accompanied by the activation of the PD-1/PD-L1 pathway, which eventually led to the massive apoptosis of T cells. Electron microscopy showed that cells showed significant apoptotic morphology. Blocking the PD-1/PD-L1 pathway can inhibit the apoptosis-inducing effect of S. maltophilia on T cells. These indicates that T cells are inhibited after being stimulated by S. maltophilia , and then accelerated to induce death without the initiation of an immunologic cascade. This paper demonstrates for the first time the inhibitory effect of S. maltophilia on cellular immunity, and the immunosuppressive effect induced by infection of S. maltophilia should be considered. [ABSTRACT FROM AUTHOR]

Endometriosis is a benign, chronic, estrogen-dependent condition, present in 10% of women of reproductive age. The condition is associated with chronic pelvic pain and infertility that influence their quality of life, as well as married life and has important socio-economic consequences. Despite its high morbidity, its etiopathogenesis is incompletely known. A large number of studies suggest that the ability of endometrial implants to grow in ectopic locations may be correlated with the altered immune response towards the endometriotic tissue. There are enough data to show that immune system mediators, such as cytokines and chemokines, are playing key roles in the onset and olso on progression of endometriosis. There are studies that prove the association between endometriosis and autoimmune diseases. The present paper aims to investigate the implications of the immune response in the etiopathogenesis of endometriosis. The study of cellular or humoral immunity deficits, the presence of autoantibodies associated with this condition, can facilitate the understanding of the mechanisms that lead to the appearance and spread of endometriosis. We hope that this information will ultimately provide the basis for the development of new effective approaches in endometriosis management. [ABSTRACT FROM AUTHOR]

Fusion (F) and Hemagglutinin-neuraminidase (HN) glycoproteins of Newcastle disease virus containing important epitopes play crucial role in stimulation of humoral and cell-mediated immunity of the host. In the present study we analyzed and compared genetic diversity of F and HN sequences related to long-term circulating sub-genotype VIIj isolates to genotype VII and II strains. In addition, F and HN epitope prediction was performed using IEDB, NetMHC 4.0 and NetMHC II 3.1 servers. Molecular docking analysis was also conducted for VIIj and LaSota isolates interacting MHC I and II molecules. Results indicated that certain specific mutations were occurred in Fusion and Hemagglutinin-neuraminidase proteins of VIIj sub-genotype. Epitope prediction study revealed that the unique variations were located on the antigenic site regions of F and HN glycoproteins. Furthermore, docking interaction analysis showed surprising results, in which defined antigenic site residues of VIIj isolates interacted to MHC molecules with higher affinity levels rather than LaSota strains used as vaccines. Our in silico results suggest that by applying certain epitope sequences inducing both immune responses, vaccination failures may be reduced and challenged vaccinated host cells may stop viral shedding beside protection from Newcastle disease infection. Thus, we recommend the introduced antigenic sites of VIIj sub-genotype in this paper would act as the great targets for epitope-based vaccine design in the region. [ABSTRACT FROM AUTHOR]

Despite the clinical success of immune checkpoint blockade, only a subset of people exhibits durable responses, suggesting that an alternative immunotherapeutic strategy is required. This paper reported a two-in-one cancer vaccine that targets programmed death ligand 1 (PDL1) that blocks the PD1/PDL1 pathway and also activates antitumor immune response. The PDL1- NitraTh vaccine, which consists of the extracellular domain of PDL1 and nitrated T cell epitope, effectively broke the immune tolerance of PDL1 and elicited PDL1-specific humoral and cellular immunity. The treatment of PDL1-NitraTh exhibited potent antitumor activity. Moreover, immunization of PDL1 vaccine increased the infiltration of tumor lymphocytes and decreased the proportion of Treg cells in tumor tissues, suggesting that the vaccine may remodel the tumor microenvironment. The upregulation of PDL1 in tumor tissues was induced by PDL1-NitraTh vaccine but not in spleen and lymphomas. This upregulation of PDL1 is beneficial to the antitumor activity of PDL1-specific humoral and cellular immunity induced by PDL1-NitraTh. In summary, PDL1-targeted vaccine exhibits potent antitumor activity and may provide an alternative immunotherapy strategy for patients who are not sensitive to PDL1 antibody drugs. [ABSTRACT FROM AUTHOR]

This paper studies the global stability of a general discrete-time viral infection model with virus-to-cell and cell-to-cell transmissions and with humoral immune response. We consider both latently and actively infected cells. The model incorporates three types of intracellular time delays. The production and clearance rates of all compartments as well as incidence rates of infection are modeled by general nonlinear functions. We use the nonstandard finite difference method to discretize the continuous-time model. We show that the solutions of the discrete-time model are positive and ultimately bounded. We derive two threshold parameters, the basic reproduction number R 0 and the humoral immune response activation number R 1 , which completely determine the existence and stability of the model's equilibria. By using Lyapunov functions, we have proven that if R 0 ≤ 1 , then the virus-free equilibrium Q0 is globally asymptotically stable; if R 1 ≤ 1 < R 0 , then the persistent infection equilibrium without immune response Q* is globally asymptotically stable; and if R 1 > 1 , then the persistent infection equilibrium with immune response Q ¯ is globally asymptotically stable. We illustrate our theoretical results by using numerical simulations. The effects of antiretroviral drug therapy and time delay on the virus dynamics are also studied. We have shown that the time delay has a similar effect as the antiretroviral drug therapy. [ABSTRACT FROM AUTHOR]

Nocardia affects immunocompromised human host exhibiting an altered cell-mediated immunity. Infectious risk after allogeneic hematopoietic cell transplantation (AHCT) is significantly correlated to the recovery status of donor-derived immune system, especially CD4+ T-cells reconstitution and thymopoiesis. The purpose of this paper is to highlight a lack of cell-mediated immunity recovery for patients presenting a nocardiosis compared to a control cohort. This is a case control retrospective monocentric study. We retrospectively analyzed a monocentric cohort of 15 cases of nocardiosis after AHCT and we explored the degree of patients' immunosuppression by phenotyping circulating lymphoid subpopulations, including NK cells, CD8+ T-cells, CD4+ T-cells and CD19+ B-cells. We focused on CD4+ T-cell subsets to appreciate thymic output, especially on naive CD4+ T-cells (NTE, CD45RA+/RO− CD4+ T-cells) and recent thymic emigrants (RTE, CD4+CD45RA+/RO−/CD31+). Infected patients were paired with a control cohort of patients with identical transplantation characteristics screened on hematological disease, AHCT conditioning, primary graft- versus -host disease (GHVD) prophylaxis, graft type, sex, age, and season at the AHCT and data concerning immunological reconstitution were compared. At onset of nocardiosis, circulating lymphocytes and CD4+ T-cells means count were respectively 730/μL and 162/μL. CD8+ T-cells, CD56+ NK cells and CD19+ B-cells means count were respectively 362/μL, 160/μL, 112/μL. CD4+ T-cells subpopulations, naïve CD4+ T-cells production was impaired with NTE and RTE means count at 26/μL and 11/μL respectively. Comparison between nocardiosis cohort and control cohort over time highlight significant lower cellular count for lymphocytes, CD4+ T-cells, NTE and RTE with p = 0.001, p < 0.001, p < 0.001, p < 0.001 respectively. Immune recovery monitoring follow-up after AHCT is of particular importance to identify patients susceptible to develop Nocardiosis. Efficient microbiological investigations toward Nocardia such PCR should be used in case of compatible clinical presentation. [ABSTRACT FROM AUTHOR]

Introduction: Smallpox has been eradicated but advances in synthetic biology have increased the risk of its re-emergence. Residual immunity in individuals who were previously vaccinated may mitigate the impact of an outbreak, but there is a high degree of uncertainty about the duration and degree of residual immunity. Both cell-mediated and humoral immunity are thought to be important but the exact mechanisms of protection are unclear. Guidelines usually suggest vaccine-induced immunity wanes to zero after 3-10 years post vaccination, whereas other estimates show long term immunity over decades.Materials and Methods: A systematic review of the literature was conducted to quantify the duration and extent of residual immunity to smallpox after vaccination.Results: Twenty-nine papers related to quantifying residual immunity to smallpox after vaccination were identified: neutralizing antibody levels were used as immune correlates of protection in 11/16 retrospective cross-sectional studies, 2/3 epidemiological studies, 6/7 prospective vaccine trials and 0/3 modeling studies. Duration of protection of >20 years was consistently shown in the 16 retrospective cross-sectional studies, while the lowest estimated duration of protection was 11.7 years among the modeling studies. Childhood vaccination conferred longer duration of protection than vaccination in adulthood, and multiple vaccinations did not appear to improve immunity.Conclusions: Most studies suggest a longer duration of residual immunity (at least 20 years) than assumed in smallpox guidelines. Estimates from modeling studies were less but still greater than the 3-10 years suggested by the WHO Committee on International Quarantine or US CDC guidelines. These recommendations were probably based on observations and studies conducted while smallpox was endemic. The cut-off values for pre-existing antibody levels of >1:20 and >1:32 reported during the period of endemic smallpox circulation may not be relevant to the contemporary population, but have been used as a threshold for identifying people with residual immunity in post-eradication era studies. Of the total antibodies produced in response to smallpox vaccination, neutralizing antibodies have shown to contribute significantly to immunological memory. Although the mechanism of immunological memory and boosting is unclear, revaccination is likely to result in a more robust response. There is a need to improve the evidence base for estimates on residual immunity to better inform planning and preparedness for re-emergent smallpox. [ABSTRACT FROM AUTHOR]

Immunosuppression is characterized by a dysfunction of humoral and/or cellular immune response leading to increase of susceptibility to secondary infections, increase of mortality and morbidity, poor productivity, and welfare and vaccination failures. Humoral immune response depression is due to perturbation of soluble factors, as complement and chemokines in innate immunity and antibodies or cytokines in adaptive immunity. At the cellular immune response, immunosuppression is the consequence of the dysfunction of T-cells, B-cells, heterophils, monocytes, macrophages, and natural Killer cells. Immunosuppression in turkeys can be caused by numerous, non-infectious, and infectious agents, having variable pathological and molecular mechanisms. Interactions between them are very complex. This paper reviews the common viruses inducing clinical and sub-clinical immunosuppression in turkeys, and enteric and neoplastic viruses in particular, as well as the interactions among them. The evaluation of immunosuppression is currently based on classical approach; however, new technique such as the microarray technology is being developed to investigate immunological mediator's genes detection. Controlling of immunosuppression include, in general, biosecurity practices, maintaining appropriate breeding conditions and vaccination of breeders and their progeny. Nevertheless, few vaccines are available against immunosuppressive viruses in turkey's industry. The development of new control strategies is reviewed. [ABSTRACT FROM AUTHOR]

[Display omitted] One of the most significant species that are present in large quantities in biological cells is reactive oxygen species (ROS). They are essential for cell motility, cell differentiation, and cellular immunity. In this paper, we introduce that (E)-1-methyl-4-(4-(propionyloxy)styryl)pyridin-1-ium (MPSPI) is an "on" type fluorescent probe regulated by the ICT mechanism. After the addition of hydrogen peroxide, the fluorophore (E)-4-(4-hydroxystyryl)-1-methylpyridin-1-ium (HMI-OH) is released. The simple probe MPSPI not only exhibited good selectivity and low cytotoxicity, but also demonstrated a detection limit as low as 35 nM and reaction times as quick as 20 s. Moreover, it has been successfully applied to the imaging of hydrogen peroxide in RAW 264.7 cells. [ABSTRACT FROM AUTHOR]

Parasite spillover from invasive aliens to native species increases the risk of disease emergence within native biota—either by direct harm to the new host or by indirect effects like increased risks of secondary infection.One example for such a detrimental effect is the parasitic copepod Mytilicola intestinalis that infected blue mussels Mytilus edulis after being introduced into the North Sea in the early 20th century. Since 1949, the parasite was blamed for multiple mass mortalities of infested blue mussels but evidence for a direct causal involvement of M. intestinalis remained circumstantial.Here, we now examine the potential effects of primary infections by the invasive parasite on the susceptibility to secondary infections with virulent bacteria (Vibrio spp.) in a full factorial infection experiment combining parasite infection (control vs. infected) with different Vibrio infection treatments (control, bath challenge, injection) in environmental conditions that either favoured the host (ambient temperature) or the bacterium (elevated temperature). The influence of primary and secondary infections on cellular immunity (phagocytosis) and Vibrio load in the haemolymph was used to correlate these results to host survival.Our results suggest that the rate of secondary Vibrio infection is increased due to lower efficiency of the cellular immune response. As a consequence, the failure of clearing Vibrio from the haemolymph might increase mortality of mussels infected by M. intestinalis.This demonstrates that indirect effects of parasite invasions can outweigh direct effects of the infection highlighting the need for a more integrative approach to understand and predict the consequences of parasite invasions. This paper demonstrates that indirect effects of immune modulation caused by infection with an invasive parasite can outweigh direct effects of the infection. This highlights the need for a more integrative approach to predict the consequences of parasite invasions and species invasions in general. [ABSTRACT FROM AUTHOR]

The goal of this paper is to investigate the dynamical behavior of a general nonlinear delayed viral infection model with cytotoxic T lymphocyte (CTL) immune response. The intrinsic growth rate of uninfected hepatocytes, incidence rate of infection, removal rate of infected hepatocytes and capsids, production and removal rate of viruses, activation rate of CTLs, and decay rate of CTLs are given by general nonlinear functions with a set of conditions on these general nonlinear functions, which make the analysis of the model more difficult. The global threshold dynamics with respect to the reproduction numbers for viral infection R0 and for CTL immune response R1 have been presented by constructing suitable Lyapunov functionals. Numerical simulations are carried out for a model with specific forms of the general functions to confirm the theoretical results and show that both the numerical and theoretical results are consistent. [ABSTRACT FROM AUTHOR]

With the HIV-1 epidemic in southern Africa still rising, a prophylactic vaccine against the region’s most prolific subtype (subtype C) would be a significant step forward. In this paper we report on the effect of 2 different adjuvants, AddaVax and AlhydroGel, formulated with HIV-1 subtype C gp140, on the development of binding and neutralising antibody titres in rabbits. AddaVax is a squalene-based oil-in-water nano-emulsion (similar to MF59) which can enhance both cellular and humoral immune responses, whilst AlhydroGel (aluminium hydroxide gel) mainly drives a Th2 response. The gp140 gene tested was derived from the superinfecting virus (SU) from participant CAP256 in the CAPRISA 002 Acute infection cohort. The furin cleavage site of the Env protein was replaced with a flexible linker and an I559P mutation introduced. Lectin affinity purified soluble Env protein was mainly trimeric as judged by molecular weight using BN-PAGE and contained intact broadly neutralising epitopes for the V3-glycan supersite (monoclonal antibodies PGT128 and PGT135), the CD4 binding site (VRC01) and the V2-glycan (PG9) but not for the trimer-specific monoclonal antibodies PG16, PGT145 and CAP256-VRC26_08. When this soluble Env protein was tested in rabbits, AlhydroGel significantly enhanced soluble Env and V1V2 binding antibodies when compared to AddaVax. Finally, AlhydroGel resulted in significantly higher neutralization titres for a subtype C Tier 1A virus (MW965.26) and increased neutralization breadth to Tier 1A and 1B viruses. However, no autologous Tier 2 neutralisation was observed. These data suggest that adjuvant selection is critical for developing a successful vaccine and AlhydroGel should be further investigated. Additional purification of trimeric native-like CAP256 Env and/or priming with DNA or MVA might enhance the induction of neutralizing antibodies and possible Tier 2 HIV-1 neutralisation. [ABSTRACT FROM AUTHOR]

We study a mathematical model of immune response by T cells where the regulatory T cells (Treg) inhibit interleukin 2 (IL‐2) secretion. We model the suppression of the autoimmune line of T cells after a different line of T cells responded to a pathogen infection. In this paper, we show that if the population of the pathogen responding line of T cells becomes large enough, the competition for IL‐2 and the increase in the death rates may lead to a depletion in the concentration of autoimmune T cells. Provided this lasts for a sufficiently long time, the concentration of autoimmune T cells can be brought down to values inside the basin of attraction of the controlled state, and autoimmunity can be suppressed. [ABSTRACT FROM AUTHOR]

Cell stability is becoming an important design concern as process technology continues to scale down. In this paper, we present a single-ended 10T SRAM cell that improves simultaneously both read static noise margin (RSNM) and write static noise margin (WSNM) by employing separate read buffer and power gating transistors, respectively. The cross-point write structure of the proposed cell facilitates bit-interleaved architecture to enhance soft-error immunity. Simulation is done on 65-nm CMOS technology on Cadence. Simulation results show that the RSNM of the proposed SRAM cell is 2.78 times and 1.47 times higher than those of the conventional 6T and Schmitt trigger-based 10T (ST-2) cells, respectively, at 0:4 V. The WSNM of the proposed design is 5.14 times larger than that of the two-port disturbfree 9T (TPDF9T) cell (without write assist) at 0:4 V. Write delay of the proposed cell is 77.56% less than that of the TPDF9T cell at 0:4 V. Leakage power dissipation of the proposed SRAM cell is 0.89 times that of the ST-2 cell at 0:4 V. The proposed cell occupies 1.34 times more area than the conventional 6T cell. [ABSTRACT FROM AUTHOR]

There has been much interest in the role of the immune system in the pathophysiology of chronic fatigue syndrome (CFS), as CFS may develop following an infection and cytokines are known to induce acute sickness behaviour, with similar symptoms to CFS. Using the PRISMA (Preferred Reporting Items for Systematic reviews and Meta-analyses) guidelines, a search was conducted on PubMed, Web of Science, Embase and PsycINFO, for CFS related-terms in combination with cytokine-related terms. Cases had to meet established criteria for CFS and be compared with healthy controls. Papers retrieved were assessed for both inclusionary criteria and quality. 38 papers met the inclusionary criteria. The quality of the studies varied. 77 serum or plasma cytokines were measured without immune stimulation. Cases of CFS had significantly elevated concentrations of transforming growth factor-beta (TGF-β) in five out of eight (63%) studies. No other cytokines were present in abnormal concentrations in the majority of studies, although insufficient data were available for some cytokines. Following physical exercise there were no differences in circulating cytokine levels between cases and controls and exercise made no difference to already elevated TGF-β concentrations. The finding of elevated TGF-β concentration, at biologically relevant levels, needs further exploration, but circulating cytokines do not seem to explain the core characteristic of post-exertional fatigue. [ABSTRACT FROM AUTHOR]

'Quantitative studies on tissue transplantation immunity. III. Actively acquired tolerance', published in Philosophical Transactions B in 1956 by Peter Medawar and his colleagues, PhD graduate Leslie Brent and postdoctoral fellow Rupert Billingham, is a full description of the concept of acquired transplantation tolerance. Their 1953 Nature paper (Billingham RE et al. 1953 Nature 172, 603-606. (doi:10.1038/172603a0)) had provided initial evidence with experimental results from a small number of neonatal mice, with mention of similar findings in chicks. The Philosophical Transactions B 1956 paper is clothed with an astonishing amount of further experimental detail. It is written in Peter Medawar's landmark style: witty, perceptive and full of images that can be recalled even when details of the supporting information have faded. Those images are provided not just by a series of 20 colour plates showing skin graft recipient mice, rats, rabbits, chickens and duck, bearing fur or plumage of donor origin, but by his choice of metaphor, simile and analogy to express the questions being addressed and the interpretation of their results, along with those of relevant published data and his prescient ideas of what the results might portend. This work influenced both immunology researchers and clinicians and helped to lay the foundations for successful transplantation programmes. It led to the award of a Nobel prize in 1960 to Medawar, and subsequently to several scientists who advanced these areas. This commentary was written to celebrate the 350th anniversary of the journal Philosophical Transactions of the Royal Society. [ABSTRACT FROM AUTHOR]

The structural elucidation of lipopolysaccharides (LPSs) from Gram‐negative marine bacteria, along with the assessment of their immunological properties, is a fascinating and active research field. Such studies can aid understanding of adaptation phenomena that occur in the marine environment, but they can also open up new perspectives on the design and development of new immunoregulatory drugs. In this paper, we report the structural characterization of the lipid A component of the LPS isolated from the marine bacterium Cobetia pacifica KMM 3879T, which is characterized by a family of structures differing in their acylation patterns. The structural assignment was achieved through extensive chemical analysis and matrix‐assisted laser desorption/ionization (MALDI) mass spectrometry. Moreover, cellular immunology studies on the LPS highlighted its low immunostimulatory impact, as well as a very interesting and promising inhibitory activity of the toxic effects of Escherichia coli LPS. [ABSTRACT FROM AUTHOR]

Based on the researches on immunoregulatory functions of Dendrobium. at home and abroad in recent years, from immune organs, immune cells, and immune molecules, this paper summarized immunoregulatory functions of polysaccharides, glycosides, and alkaloids extracted from Dendrobium. on the body, including reducing the inflammation, inhibiting tumor, and slowing down aging, to provide theoretical references for in-depth researches and development of modern biotechnology for Dendrobium. [ABSTRACT FROM AUTHOR]

Chronicity in wound healing is a challenge for health services financially and scientifically, with negative consequences on patients' lives. This paper seeks to explore why chronic wounds fail to heal in relation to the inflammatory cellular dysfunction associated with bioflm development. Findings demonstrate an association between chronic wounds failing to heal, the presence of devitalised tissue and abnormal immune cell activity with a consequential excessive release of harmful matrix metalloproteases (MMPs). This process perpetuates the cycle of wound chronicity and extracellular matrix destruction, which prolongs the inflammatory response, fuelling biofilm formation. Evidence suggests that 'trapping' MMPs may increase new tissue growth but, while devitalised tissue is present, phagocytic cells continue to secrete MMPs and chronicity persists. Consequently, by removing the trigger and implementing effective, sustained debridement of devitalised tissue, both MMP and biofilm production will be diminished, with positive healing outcomes. [ABSTRACT FROM AUTHOR]

Iran is the only country in the world currently with a legalized compensated kidney donation system, in which kidney sellers are matched with end‐stage renal disease patients through a regulated process. From a practical point of view, this model provides an abundance of kidneys for transplantation as opposed to the American model that relies on altruistic donation. The major concern about adopting the Iranian model is the possibility of exploitation. A large body of literature exists on this topic, but few have focused on its cultural aspects. This paper sheds light on the cultural implications of the Iranian model by providing empirical evidence on the social stigmas against kidney sale in Iran. We claim that these stigmas act as barriers to entry to the supply market of kidneys. Due to the conditions created by social stigmas, kidney sellers are forced to consider not only monetary rewards but also cultural factors. Thus, they tend to be more cautious and try to avoid impulsive decisions. Such social stigmas act as unofficial regulatory forces to keep kidney sale as the last resort for the poor, to diversify the supply market by age, and to stretch the decision‐making process in the absence of a mandatory waiting period for transplantation. [ABSTRACT FROM AUTHOR]

Obesity and depression are among the most pressing health problems in the contemporary world. Obesity and depression share a bidirectional relationship, whereby each condition increases the risk of the other. By inference, shared pathways may underpin the comorbidity between obesity and depression. Activation of cell-mediated immunity (CMI) is a key factor in the pathophysiology of depression. CMI cytokines, including IFN-γ, TNFα and IL-1β, induce the catabolism of tryptophan (TRY) by stimulating indoleamine 2,3-dioxygenase (IDO) resulting in the synthesis of kynurenine (KYN) and other tryptophan catabolites (TRYCATs). In the CNS, TRYCATs have been related to oxidative damage, inflammation, mitochondrial dysfunction, cytotoxicity, excitotoxicity, neurotoxicity and lowered neuroplasticity. The pathophysiology of obesity is also associated with a state of aberrant inflammation that activates aryl hydrocarbon receptor (AHR), a pathway involved in the detection of intracellular or environmental changes as well as with increases in the production of TRYCATs, being KYN an agonists of AHR. Both AHR and TRYCATS are involved in obesity and related metabolic disorders. These changes in the TRYCAT pathway may contribute to the onset of neuropsychiatric symptoms in obesity. This paper reviews the role of immune activation, IDO stimulation and increased TRYCAT production in the pathophysiology of depression and obesity. Here we suggest that increased synthesis of detrimental TRYCATs is implicated in comorbid obesity and depression and is a new drug target to treat both diseases. [ABSTRACT FROM AUTHOR]

In this paper the development and current status of Neuroimmune Biology (NIB) is summarised and the extended NISS is discussed. The significance of this newly emerging science is the demonstration that NISS coordinates host defence against infection and other pathogenic agents. Indeed NISS is in control of the biology of higher organisms for their life time. [ABSTRACT FROM AUTHOR]

Direct cell-to-cell transmission of HIV-1 is proved to be a more efficient means of virus infection than virus-to-cell transmission. In this paper, we incorporate both virus-to-cell and cell-to-cell transmissions into an HIV-1 virus model, which also contains intracellular delay and humoral immunity. By analyzing the characteristic equations, the local stability of feasible equilibria is established. By using Lyapunov functionals and LaSalle’s invariance principle, it is verified that global threshold dynamics of the model can be explicitly described by immune-inactivated reproduction rate and immune-activated reproduction rate. Numerical simulations are carried out to illustrate the corresponding theoretical results. [ABSTRACT FROM AUTHOR]

Highlights: [•] The manuscript describes our view on hemocyte subsets, lineages and compartments. [•] The paper details the plasticity of plasmatocyte/macrophage lineages. [•] One of the main points of the paper is the regulation of the cell mediated immunity. [•] Phenotypic and functional changes upon effector cell differentiation are described. [•] The ontogenesis of the hematopoietic compartments is presented. [ABSTRACT FROM AUTHOR]

Indoleamine 2,3-dioxygenase 1 (IDO1), the L-tryptophan-degrading enzyme, plays a key role in the immunomodulatory effects on several types of immune cells. Originally known for its regulatory function during pregnancy and chronic inflammation in tumorigenesis, the activity of IDO1 seems to modify the inflammatory state of infectious diseases. The pathophysiologic activity of L-tryptophan metabolites, kynurenines, is well recognized. Therefore, an understanding of the regulation of IDO1 and the subsequent biochemical reactions is essential for the design of therapeutic strategies in certain immune diseases. In this paper, current knowledge about the role of IDO1 and its metabolites during various infectious diseases is presented. Particularly, the regulation of type I interferons (IFNs) production via IDO1 in virus infection is discussed. This paper offers insights into new therapeutic strategies in the modulation of viral infection and several immune-related disorders. [ABSTRACT FROM AUTHOR]