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10.1084/jem.20212553

http://scihub22266oqcxt.onion/10.1084/jem.20212553
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35420627!9014793!35420627
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suck abstract from ncbi


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pmid35420627      J+Exp+Med 2022 ; 219 (6): ä
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  • SARS-CoV-2 infection relaxes peripheral B cell tolerance #MMPMID35420627
  • Castleman MJ; Stumpf MM; Therrien NR; Smith MJ; Lesteberg KE; Palmer BE; Maloney JP; Janssen WJ; Mould KJ; Beckham JD; Pelanda R; Torres RM
  • J Exp Med 2022[Jun]; 219 (6): ä PMID35420627show ga
  • Severe SARS-CoV-2 infection is associated with strong inflammation and autoantibody production against diverse self-antigens, suggesting a system-wide defect in B cell tolerance. BND cells are a B cell subset in healthy individuals harboring autoreactive but anergic B lymphocytes. In vitro evidence suggests inflammatory stimuli can breach peripheral B cell tolerance in this subset. We asked whether SARS-CoV-2-associated inflammation impairs BND cell peripheral tolerance. To address this, PBMCs and plasma were collected from healthy controls, individuals immunized against SARS-CoV-2, or subjects with convalescent or severe SARS-CoV-2 infection. We demonstrate that BND cells from severely infected individuals are significantly activated, display reduced inhibitory receptor expression, and restored BCR signaling, indicative of a breach in anergy during viral infection, supported by increased levels of autoreactive antibodies. The phenotypic and functional BND cell alterations significantly correlate with increased inflammation in severe SARS-CoV-2 infection. Thus, autoreactive BND cells are released from peripheral tolerance with SARS-CoV-2 infection, likely as a consequence of robust systemic inflammation.
  • |*COVID-19[MESH]
  • |*Peripheral Tolerance[MESH]
  • |Antibodies, Viral[MESH]
  • |B-Lymphocytes[MESH]
  • |Humans[MESH]
  • |Inflammation/metabolism[MESH]


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