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10.1172/JCI151520 http://scihub22266oqcxt.onion/10.1172/JCI151520 34437303!8516454!34437303     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       J+Clin+Invest 2021 ; 131 (20): ä Nephropedia Template TP {{tp|p=34437303|t=2021. The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children |pdf=|usr=}}{{34437303}} gab.com Text The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=34437303 #FOAvip Multisystem inflammatory syndrome in children (MIS-C) manifests as a severe and uncontrolled inflammatory response with multiorgan involvement, occurring weeks after SARS-CoV-2 infection. Here, we utilized proteomics, RNA sequencing, autoantibody arrays, and B cell receptor (BCR) repertoire analysis to characterize MIS-C immunopathogenesis and identify factors contributing to severe manifestations and intensive care unit admission. Inflammation markers, humoral immune responses, neutrophil activation, and complement and coagulation pathways were highly enriched in MIS-C patient serum, with a more hyperinflammatory profile in severe than in mild MIS-C cases. We identified a strong autoimmune signature in MIS-C, with autoantibodies targeted to both ubiquitously expressed and tissue-specific antigens, suggesting autoantigen release and excessive antigenic drive may result from systemic tissue damage. We further identified a cluster of patients with enhanced neutrophil responses as well as high anti-Spike IgG and autoantibody titers. BCR sequencing of these patients identified a strong imprint of antigenic drive with substantial BCR sequence connectivity and usage of autoimmunity-associated immunoglobulin heavy chain variable region (IGHV) genes. This cluster was linked to a TRBV11-2 expanded T cell receptor (TCR) repertoire, consistent with previous studies indicating a superantigen-driven pathogenic process. Overall, we identify a combination of pathogenic pathways that culminate in MIS-C and may inform treatment. Twit Text FOAVip The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=34437303 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34437303 #FOAvip English Wikipedia <ref>{{Cite pmid|34437303}}</ref> The autoimmune signature of hyperinflammatory multisystem inflammatory syndrome in children #MMPMID34437303 Porritt RA; Binek A; Paschold L; Rivas MN; McArdle A; Yonker LM; Alter G; Chandnani HK; Lopez M; Fasano A; Van Eyk JE; Binder M; Arditi M J Clin Invest 2021[Oct]; 131 (20): ä PMID34437303show ga Multisystem inflammatory syndrome in children (MIS-C) manifests as a severe and uncontrolled inflammatory response with multiorgan involvement, occurring weeks after SARS-CoV-2 infection. Here, we utilized proteomics, RNA sequencing, autoantibody arrays, and B cell receptor (BCR) repertoire analysis to characterize MIS-C immunopathogenesis and identify factors contributing to severe manifestations and intensive care unit admission. Inflammation markers, humoral immune responses, neutrophil activation, and complement and coagulation pathways were highly enriched in MIS-C patient serum, with a more hyperinflammatory profile in severe than in mild MIS-C cases. We identified a strong autoimmune signature in MIS-C, with autoantibodies targeted to both ubiquitously expressed and tissue-specific antigens, suggesting autoantigen release and excessive antigenic drive may result from systemic tissue damage. We further identified a cluster of patients with enhanced neutrophil responses as well as high anti-Spike IgG and autoantibody titers. BCR sequencing of these patients identified a strong imprint of antigenic drive with substantial BCR sequence connectivity and usage of autoimmunity-associated immunoglobulin heavy chain variable region (IGHV) genes. This cluster was linked to a TRBV11-2 expanded T cell receptor (TCR) repertoire, consistent with previous studies indicating a superantigen-driven pathogenic process. Overall, we identify a combination of pathogenic pathways that culminate in MIS-C and may inform treatment. |*Autoimmunity[MESH] |Adaptive Immunity[MESH] |Adolescent[MESH] |Biomarkers/metabolism[MESH] |COVID-19/*complications/genetics/immunology/metabolism[MESH] |Case-Control Studies[MESH] |Child[MESH] |Child, Preschool[MESH] |Cohort Studies[MESH] |Cytokine Release Syndrome/immunology[MESH] |Female[MESH] |Humans[MESH] |Infant[MESH] |Inflammation/immunology[MESH] |Male[MESH] |Mucocutaneous Lymph Node Syndrome/genetics/immunology/metabolism[MESH] |Neutrophil Activation[MESH] |Proteomics[MESH] |RNA-Seq[MESH] |Receptors, Antigen, B-Cell/genetics[MESH] |Severity of Illness Index[MESH]The autoimmune signature of hyperinflammatory multisystem inflammatory(epmc).pdf DeepDyve Pubget Overpricing