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10.4049/jimmunol.1600017

http://scihub22266oqcxt.onion/10.4049/jimmunol.1600017
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C4868625!4868625!27022196
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suck abstract from ncbi


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pmid27022196      J+Immunol 2016 ; 196 (9): 3525-31
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  • BAFF promotes autoantibody production via TACI-dependent activation of transitional B cells #MMPMID27022196
  • Jacobs HM; Thouvenel CD; Leach S; Arkatkar T; Metzler G; Scharping NE; Kolhatkar NS; Rawlings DJ; Jackson SW
  • J Immunol 2016[May]; 196 (9): 3525-31 PMID27022196show ga
  • Mice overexpressing B cell activating factor of the TNF family (BAFF) develop systemic autoimmunity characterized by class-switched anti-nuclear antibodies. Transmembrane activator and CAML interactor (TACI) signals are critical for BAFF-mediated autoimmunity, but the B cell developmental subsets undergoing TACI-dependent activation in settings of excess BAFF remains unclear. We now report that, whereas surface TACI expression is usually limited to mature B cells, excess BAFF promotes the expansion of TACI-expressing transitional B cells. TACIhi transitional cells from BAFF-Tg mice are characterized by an activated, cycling phenotype; and the TACIhi cell subset is specifically enriched for autoreactivity, expresses activation-induced cytidine deaminase (AID) and T-bet and exhibits evidence of somatic hypermutation. Consistent with a potential contribution to BAFF-mediated humoral autoimmunity, TACIhi transitional B cells from BAFF-Tg mice spontaneously produce class-switched autoantibodies ex vivo. These combined findings highlight a novel mechanism whereby BAFF promotes humoral autoimmunity via direct, TACI-dependent activation of transitional B cells.
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