#AIBD2016 P-098 Epidemiology and Risk Factors of IgA Nephropathy in Patients with IBD https://t.co/9kyLJvIne3
Mucosal Immunity
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This population-based study of patients with head and neck cancer investigates whether immunologic response to human papillomavirus 16 is associated with patien
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Abstract Fc receptor-like (FcRL) proteins are a family of cellular receptors homologous to FcγRI and are predominantly expressed by B cells. They function to costimulate or inhibi..
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AIDS Res Ther. 2016 Apr 11;13(1):19. Review
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A new study has found that genes and early environment play big roles in shaping the gut microbiome.
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A large set of microbial metabolic models (AGORA) could be applied to better understand the functions of the human gut microbiome.
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Different types of tears under a light microscope.
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Secretory IgA (SIgA) is one important line of defense in intestinal mucosal surface to protect the intestinal epithelium from enteric toxins and pathogenic microorganisms. Multiple factors, such as intestinal microbiota, intestinal cytokines and nutrients, are highly involved in intestinal production of SIgA. Recently, glutamine has been shown to affect intestinal SIgA production, however, the underlying mechanism by which glutamine promotes intestinal SIgA secretion remains to know. Here, we review the current knowledge regarding glutamine in intestinal immunity, and show that glutamine enhances intestinal SIgA production may through intestinal microbiota, intestinal antigen sampling and presentation, induction pathways for SIgA production by plasma cells (both T-dependent and T-independent pathway), and even SIgA transportation. Altogether, the glutamine-intestinal SIgA axis has broad therapeutic implications for intestinal SIgA -associated diseases, such as celiac disease, allergy, and inflammatory bowel disease.
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Understanding the host immune response to vaginal exposure to RNA viruses is required to combat sexual transmission of this class of pathogens. In this study, using lymphocytic choriomeningitis virus (LCMV) and Zika virus (ZIKV) in wild-type mice, we show that these viruses replicate in the vaginal mucosa with minimal induction of antiviral interferon and inflammatory response, causing dampened innate-mediated control of viral replication and a failure to mature local antigen-presenting cells (APCs). Enhancement of innate-mediated inflammation in the vaginal mucosa rescues this phenotype and completely inhibits ZIKV replication. To gain a better understanding of how this dampened innate immune activation in the lower female reproductive tract may also affect adaptive immunity, we modeled CD8 T cell responses using vaginal LCMV infection. We show that the lack of APC maturation in the vaginal mucosa leads to a delay in CD8 T cell activation in the draining lymph node and hinders the timely appearance of effector CD8 T cells in vaginal mucosa, thus further delaying viral control in this tissue. Our study demonstrates that vaginal tissue is exceptionally vulnerable to infection by RNA viruses and provides a conceptual framework for the male to female sexual transmission observed during ZIKV infection. Via Kenzibit
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Mammalian evolution has occurred in the presence of mutualistic, commensal, and pathogenic
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Two body systems thought to be functionally separate have been found to be connected through gut bacteria. From Oregon State University, scientists identif
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Mucosal Immunol. 2016 Dec 7. doi: 10.1038/mi.2016.103. [Epub ahead of print]
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In several clinical trials, the probiotic bacterium Lactobacillus paracasei DG has been shown to promote health, but until now, the mechanism has remained a black box.
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J Am Soc Nephrol. 2016 Nov 7. pii: ASN.2016060640. [Epub ahead of print]
Gilbert C FAURE's insight:
doesn'twork?
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Transplantation. 2016 Sep;100(9):1955-62. doi: 10.1097/TP.0000000000000962.
Gilbert C FAURE's insight:
IgA nephropathy
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Gilbert C FAURE's insight:
Toronto 2016, thank you Jiri Mestecky Tom Mac Donald inside
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How tissue-specific anatomical distribution and phenotypic specialization are linked to protective efficacy of memory T cells against reinfection is unclear. Here, we show that lung environmental cues program recently recruited central-like memory cells with migratory potentials for their tissue-specific functions during lethal respiratory virus infection. After entering the lung, some central-like cells retain their original CD27hiCXCR3hi phenotype, enabling them to localize near the infected bronchiolar epithelium and airway lumen to function as the first line of defense against pathogen encounter. Others, in response to local cytokine triggers, undergo a secondary program of differentiation that leads to the loss of CXCR3, migration arrest, and clustering within peribronchoarterial areas and in interalveolar septa. Here, the immune system adapts its response to prevent systemic viral dissemination and mortality. These results reveal the striking and unexpected spatial organization of central- versus effector-like memory cells within the lung and how cooperation between these two subsets contributes to host defense.
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Gilbert C FAURE's insight:
Th17 cells accumulate in the gut, where they mediate barrier defenses and repair but can also provoke inflammatory disease. In mice, segmented filamentous bacteria (SFB) is sufficient to induce Th17 cells in the gut, but functionally analogous microbes in humans have not been defined. Here, we identified Bifidobacterium adolescentis as one of several human symbiont bacterial species that could, alone, induce Th17 cells in the small intestine of mice. B. adolescentis and SFB exhibited overlapping but also distinct activities, suggesting multiple routes to intestinal Th17 induction. Like SFB, B. adolescentis exacerbated autoimmune arthritis, arguing for its pathological relevance. Our results help to inform the search for therapeutic targets in diseases associated with Th17 responses and mucosal dysfunction.
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Epigenetic perturbations may be an important factor in diseases where both genes and environment play a role.
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Inflamm Res. 2016 Nov 22. [Epub ahead of print] Review
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chinese metaanalysis
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By photolabelling intestinal cells, Krebs and colleagues provide direct evidence that
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