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10.1172/JCI146614 http://scihub22266oqcxt.onion/10.1172/JCI146614 33705359!8121516!33705359     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2021 ; 131 (10): ä Nephropedia Template TP {{tp|p=33705359|t=2021. HLA class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children |pdf=|usr=}}{{33705359}} gab.com Text HLA class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=33705359 #FOAvip Multisystem inflammatory syndrome in children (MIS-C), a hyperinflammatory syndrome associated with SARS-CoV-2 infection, shares clinical features with toxic shock syndrome, which is triggered by bacterial superantigens. Superantigen specificity for different Vbeta chains results in Vbeta skewing, whereby T cells with specific Vbeta chains and diverse antigen specificity are overrepresented in the T cell receptor (TCR) repertoire. Here, we characterized the TCR repertoire of MIS-C patients and found a profound expansion of TCRbeta variable gene 11-2 (TRBV11-2), with up to 24% of clonal T cell space occupied by TRBV11-2 T cells, which correlated with MIS-C severity and serum cytokine levels. Analysis of TRBJ gene usage and complementarity-determining region 3 (CDR3) length distribution of MIS-C expanded TRBV11-2 clones revealed extensive junctional diversity. Patients with TRBV11-2 expansion shared HLA class I alleles A02, B35, and C04, indicating what we believe is a novel mechanism for CDR3-independent T cell expansion. In silico modeling indicated that polyacidic residues in the Vbeta chain encoded by TRBV11-2 (Vbeta21.3) strongly interact with the superantigen-like motif of SARS-CoV-2 spike glycoprotein, suggesting that unprocessed SARS-CoV-2 spike may directly mediate TRBV11-2 expansion. Overall, our data indicate that a CDR3-independent interaction between SARS-CoV-2 spike and TCR leads to T cell expansion and possibly activation, which may account for the clinical presentation of MIS-C. Twit Text FOAVip HLA class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=33705359 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33705359 #FOAvip English Wikipedia <ref>{{Cite pmid|33705359}}</ref> HLA class I-associated expansion of TRBV11-2 T cells in multisystem inflammatory syndrome in children #MMPMID33705359 Porritt RA; Paschold L; Rivas MN; Cheng MH; Yonker LM; Chandnani H; Lopez M; Simnica D; Schultheiss C; Santiskulvong C; Van Eyk J; McCormick JK; Fasano A; Bahar I; Binder M; Arditi M J Clin Invest 2021[May]; 131 (10): ä PMID33705359show ga Multisystem inflammatory syndrome in children (MIS-C), a hyperinflammatory syndrome associated with SARS-CoV-2 infection, shares clinical features with toxic shock syndrome, which is triggered by bacterial superantigens. Superantigen specificity for different Vbeta chains results in Vbeta skewing, whereby T cells with specific Vbeta chains and diverse antigen specificity are overrepresented in the T cell receptor (TCR) repertoire. Here, we characterized the TCR repertoire of MIS-C patients and found a profound expansion of TCRbeta variable gene 11-2 (TRBV11-2), with up to 24% of clonal T cell space occupied by TRBV11-2 T cells, which correlated with MIS-C severity and serum cytokine levels. Analysis of TRBJ gene usage and complementarity-determining region 3 (CDR3) length distribution of MIS-C expanded TRBV11-2 clones revealed extensive junctional diversity. Patients with TRBV11-2 expansion shared HLA class I alleles A02, B35, and C04, indicating what we believe is a novel mechanism for CDR3-independent T cell expansion. In silico modeling indicated that polyacidic residues in the Vbeta chain encoded by TRBV11-2 (Vbeta21.3) strongly interact with the superantigen-like motif of SARS-CoV-2 spike glycoprotein, suggesting that unprocessed SARS-CoV-2 spike may directly mediate TRBV11-2 expansion. Overall, our data indicate that a CDR3-independent interaction between SARS-CoV-2 spike and TCR leads to T cell expansion and possibly activation, which may account for the clinical presentation of MIS-C. |COVID-19/genetics/*immunology[MESH] |Child[MESH] |Complementarity Determining Regions/genetics/*immunology[MESH] |Female[MESH] |Histocompatibility Antigens Class I/genetics/*immunology[MESH] |Humans[MESH] |Male[MESH] |Receptors, Antigen, T-Cell, alpha-beta/genetics/*immunology[MESH] |SARS-CoV-2/genetics/*immunology[MESH] |Spike Glycoprotein, Coronavirus/genetics/*immunology[MESH] |Systemic Inflammatory Response Syndrome/genetics/*immunology[MESH]HLA class I-associated expansion of TRBV11-2 T cells in multisystem in(epmc).pdf DeepDyve Pubget Overpricing