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      Chronic intestinal inflammatory condition generates IL-10-producing regulatory B cell subset characterized by CD1d upregulation.

      Immunity
      Animals, Antigens, CD1, genetics, immunology, Antigens, CD1d, B-Lymphocyte Subsets, Chronic Disease, Colitis, pathology, Colon, Disease Progression, Female, Interleukin-10, biosynthesis, Lymphoid Tissue, cytology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Up-Regulation

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          Abstract

          B cells possess a variety of immune functions that are involved in normal and abnormal immune responses, including autoimmune disorders. Through murine models of intestinal inflammation, we here demonstrate a B cell subset that is induced in gut-associated lymphoid tissues and is characterized by CD1d upregulation. This B cell subset appears under a chronic inflammatory environment, produces IL-10, and suppresses progression of intestinal inflammation by downregulating inflammatory cascades associated with IL-1 upregulation and STAT3 activation rather than by altering polarized T helper responses. This study indicates that B cells, by producing cytokines such as IL-10, can act as regulatory cells in immunologically mediated inflammatory reactions.

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