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10.3390/jcm6020013

http://scihub22266oqcxt.onion/10.3390/jcm6020013
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C5332917!5332917!28134752
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suck abstract from ncbi


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pmid28134752      J+Clin+Med 2017 ; 6 (2): ä
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  • Mechanisms by Which B Cells and Regulatory T Cells Influence Development of Murine Organ-Specific Autoimmune Diseases #MMPMID28134752
  • Ellis JS; Braley-Mullen H
  • J Clin Med 2017[Feb]; 6 (2): ä PMID28134752show ga
  • Experiments with B cell-deficient (B?/?) mice indicate that a number of autoimmune diseases require B cells in addition to T cells for their development. Using B?/? Non-obese diabetic (NOD) and NOD.H-2h4 mice, we demonstrated that development of spontaneous autoimmune thyroiditis (SAT), Sjogren?s syndrome and diabetes do not develop in B?/? mice, whereas all three diseases develop in B cell-positive wild-type (WT) mice. B cells are required early in life, since reconstitution of adult mice with B cells or autoantibodies did not restore their ability to develop disease. B cells function as important antigen presenting cells (APC) to initiate activation of autoreactive CD4+ effector T cells. If B cells are absent or greatly reduced in number, other APC will present the antigen, such that Treg are preferentially activated and effector T cells are not activated. In these situations, B?/? or B cell-depleted mice develop the autoimmune disease when T regulatory cells (Treg) are transiently depleted. This review focuses on how B cells influence Treg activation and function, and briefly considers factors that influence the effectiveness of B cell depletion for treatment of autoimmune diseases.
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