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Plasticity of TH17 cells in Peyer's patches is responsible for the induction of T cell–dependent IgA responses | Nature Immunology
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Nature Immunology - IgA is essential in the maintenance of mucosal host defense and intestinal homeostasis. Stockinger and colleagues show that TH17 cells acquire a follicular helper T cell...
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headline:Plasticity of TH17 cells in Peyer's patches is responsible for the induction of T cellâdependent IgA responses
description:IgA is essential in the maintenance of mucosal host defense and intestinal homeostasis. Stockinger and colleagues show that TH17 cells acquire a follicular helper T cell phenotype in Peyer's patches and induce the development of IgA-producing B cells. Intestinal Peyer's patches are essential lymphoid organs for the generation of T cellâdependent immunoglobulin A (IgA) for gut homeostasis. Through the use of interleukin 17 (IL-17) fate-reporter mice, we found here that endogenous cells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'preferentially' homed to the intestines and were maintained independently of IL-23. In Peyer's patches, such TH17 cells acquired a follicular helper T cell (TFH cell) phenotype and induced the development of IgA-producing germinal center B cells. Mice deficient in TH17 cells failed to generate antigen-specific IgA responses, which provides evidence that TH17 cells are the crucial subset required for the production of high-affinity T cellâdependent IgA.
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headline:Plasticity of TH17 cells in Peyer's patches is responsible for the induction of T cellâdependent IgA responses
description:IgA is essential in the maintenance of mucosal host defense and intestinal homeostasis. Stockinger and colleagues show that TH17 cells acquire a follicular helper T cell phenotype in Peyer's patches and induce the development of IgA-producing B cells. Intestinal Peyer's patches are essential lymphoid organs for the generation of T cellâdependent immunoglobulin A (IgA) for gut homeostasis. Through the use of interleukin 17 (IL-17) fate-reporter mice, we found here that endogenous cells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'preferentially' homed to the intestines and were maintained independently of IL-23. In Peyer's patches, such TH17 cells acquired a follicular helper T cell (TFH cell) phenotype and induced the development of IgA-producing germinal center B cells. Mice deficient in TH17 cells failed to generate antigen-specific IgA responses, which provides evidence that TH17 cells are the crucial subset required for the production of high-affinity T cellâdependent IgA.
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