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10.1038/nri.2017.24

http://scihub22266oqcxt.onion/10.1038/nri.2017.24
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C5523822!5523822!28393923
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suck abstract from ncbi

pmid28393923      Nat+Rev+Immunol 2017 ; 17 (7): 421-36
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  • Altered B cell signalling in autoimmunity #MMPMID28393923
  • Rawlings DJ; Metzler G; Wray-Dutra M; Jackson SW
  • Nat Rev Immunol 2017[Jul]; 17 (7): 421-36 PMID28393923show ga
  • Recent work has provided new insights into how altered B cell-intrinsic signals ? through the B cell receptor (BCR) and key co-receptors ? function together to promote the pathogenesis of autoimmunity. These combined signals affect B cells at two distinct stages: first, in the selection of the naive repertoire; and second, during extrafollicular or germinal centre activation responses. Thus, dysregulated signalling can lead to both an altered naive BCR repertoire and the generation of autoantibody-producing B cells. Strikingly, high-affinity autoantibodies predate and predict disease in several autoimmune disorders, including type 1 diabetes and systemic lupus erythematosus. This Review summarizes how, rather than being a downstream consequence of autoreactive T cell activation, dysregulated B cell signalling can function as a primary driver of many human autoimmune diseases.
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