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      A dominant, coordinated T regulatory cell-IgA response to the intestinal microbiota.

      Proceedings of the National Academy of Sciences of the United States of America

      Animals, Antigens, Bacterial, immunology, B-Lymphocytes, Flagellin, Forkhead Transcription Factors, Immunoglobulin A, biosynthesis, Interleukin-2 Receptor alpha Subunit, Intestines, microbiology, Lymphocyte Depletion, Mice, Mice, Transgenic, Mucous Membrane, Receptors, Antigen, T-Cell, alpha-beta, genetics, T-Lymphocytes, Regulatory

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          Abstract

          A T cell receptor transgenic mouse line reactive to a microbiota flagellin, CBir1, was used to define mechanisms of host microbiota homeostasis. Intestinal IgA, but not serum IgA, was found to block mucosal flagellin uptake and systemic T cell activation in mice. Depletion of CD4(+)CD25(+) Tregs decreased IgA(+) B cells, total IgA, and CBir1-specific IgA in gut within days. Repletion of T cell-deficient mice with either CD4(+)CD25(+) or CD4(+)foxp3(+) Tregs restored intestinal IgA to a much greater extent than their reciprocal CD4(+) subsets, indicating that Tregs are the major helper cells for IgA responses to microbiota antigens such as flagellin. We propose that the major role of this coordinated Treg-IgA response is to maintain commensalism with the microbiota.

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          Author and article information

          Journal
          19889972
          2780781
          10.1073/pnas.0812681106

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