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10.1084/jem.20212553 http://scihub22266oqcxt.onion/10.1084/jem.20212553 35420627!9014793!35420627     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\35420627.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Exp+Med 2022 ; 219 (6): ä Nephropedia Template TP {{tp|p=35420627|t=2022. SARS-CoV-2 infection relaxes peripheral B cell tolerance |pdf=|usr=}}{{35420627}} gab.com Text SARS-CoV-2 infection relaxes peripheral B cell tolerance JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=35420627 #FOAvip 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. Twit Text FOAVip SARS-CoV-2 infection relaxes peripheral B cell tolerance ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=35420627 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35420627 #FOAvip English Wikipedia <ref>{{Cite pmid|35420627}}</ref> 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]SARS-CoV-2 infection relaxes peripheral B cell tolerance (epmc).pdf DeepDyve Pubget Overpricing