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      T H17 cell plasticity in Peyer’s patches is responsible for induction of T cell-dependent IgA responses

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          Abstract

          Intestinal Peyer’s patches are essential lymphoid organs for the generation of T cell-dependent immunoglobulin (Ig) A production for gut homeostasis. Using IL-17 fate reporter mice we show here that endogenous T H17 cells in lymphoid organs of naïve mice home preferentially to the intestine and are maintained independently of IL-23. In Peyer’s patches such T H17 cells acquire a T follicular helper (T FH) phenotype and induce the development of IgA-producing germinal center B cells. Mice deficient in T H17 cells fail to generate antigen specific IgA responses, providing evidence that T H17 cells are the crucial subset required for high affinity T cell-dependent IgA production.

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          Differential roles of interleukin-17A and -17F in host defense against mucoepithelial bacterial infection and allergic responses.

          Harumichi Ishigame, Shigeru Kakuta, Takeshi Nagai … (2009)
          Interleukin-17A (IL-17A) is a cytokine produced by T helper 17 (Th17) cells and plays important roles in the development of inflammatory diseases. Although IL-17F is highly homologous to IL-17A and binds the same receptor, the functional roles of this molecule remain largely unknown. Here, we demonstrated with Il17a(-/-), Il17f(-/-), and Il17a(-/-)Il17f(-/-) mice that IL-17F played only marginal roles, if at all, in the development of delayed-type and contact hypersensitivities, autoimmune encephalomyelitis, collagen-induced arthritis, and arthritis in Il1rn(-/-) mice. In contrast, both IL-17F and IL-17A were involved in host defense against mucoepithelial infection by Staphylococcus aureus and Citrobacter rodentium. IL-17A was produced mainly in T cells, whereas IL-17F was produced in T cells, innate immune cells, and epithelial cells. Although only IL-17A efficiently induced cytokines in macrophages, both cytokines activated epithelial innate immune responses. These observations indicate that IL-17A and IL-17F have overlapping yet distinct roles in host immune and defense mechanisms.
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            The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo.

            Mandy McGeachy, Yi. Chen, Cristina Tato … (2009)
            Interleukin 23 (IL-23) is required for autoimmune inflammation mediated by IL-17-producing helper T cells (T(H)-17 cells) and has been linked to many human immune disorders. Here we restricted deficiency in the IL-23 receptor to defined cell populations in vivo to investigate the requirement for IL-23 signaling in the development and function of T(H)-17 cells in autoimmunity, inflammation and infection. In the absence of IL-23, T(H)-17 development was stalled at the early activation stage. T(H)-17 cells failed to downregulate IL-2 and also failed to maintain IL-17 production or upregulate expression of the IL-7 receptor alpha-chain. These defects were associated with less proliferation; consequently, fewer effector T(H)-17 cells were produced in the lymph nodes and hence available to emigrate to the bloodstream and tissues.
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              Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut.

              Keiichiro Suzuki, Bob Meek, Yasuko Doi … (2004)
              The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID(-/-) mice. Reconstitution of lamina propria IgA production in AID(-/-) mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 100941354
                Journal ID (pubmed-jr-id): 21750
                Journal ID (nlm-ta): Nat Immunol
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Print): 1529-2908
                ISSN (Electronic): 1529-2916
                Publication date Nihms-submitted: 28 January 2013
                Publication date (Electronic): 10 March 2013
                Publication date (Print): April 2013
                Publication date PMC-release: 01 October 2013
                Volume: 14
                Issue: 4
                Pages: 372-379
                Affiliations
                [1 ]Division of Molecular Immunology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK
                [3 ]Department of Lymphocyte Physiology, IGC , P-2781-901 Oeiras, Portugal
                [4 ]III. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Germany
                Author notes
                [2]

                Present affiliation: Department of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Suita565-0871, Japan

                [*]

                these authors contributed equally

                Article
                Manuscript ID: EMS51382
                DOI: 10.1038/ni.2552
                PMC ID: 3672955
                PubMed ID: 23475182
                SO-VID: 86e49c20-1048-43d1-a534-cce962e38750
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: Medical Research Council :
                Award ID: U.1175.02.003.00003(60535) || MRC_
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

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