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10.1084/jem.20211381 http://scihub22266oqcxt.onion/10.1084/jem.20211381 34914824!8685281!34914824     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34914824&cmd=llinks): Failed to open stream: HTTP request failed! 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TIM3+ TRBV11-2 T cells and IFNgamma signature in patrolling monocytes and CD16+ NK cells delineate MIS-C |pdf=|usr=}}{{34914824}} gab.com Text TIM3+ TRBV11-2 T cells and IFNgamma signature in patrolling monocytes and CD16+ NK cells delineate MIS-C JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=34914824 #FOAvip In rare instances, pediatric SARS-CoV-2 infection results in a novel immunodysregulation syndrome termed multisystem inflammatory syndrome in children (MIS-C). We compared MIS-C immunopathology with severe COVID-19 in adults. MIS-C does not result in pneumocyte damage but is associated with vascular endotheliitis and gastrointestinal epithelial injury. In MIS-C, the cytokine release syndrome is characterized by IFNgamma and not type I interferon. Persistence of patrolling monocytes differentiates MIS-C from severe COVID-19, which is dominated by HLA-DRlo classical monocytes. IFNgamma levels correlate with granzyme B production in CD16+ NK cells and TIM3 expression on CD38+/HLA-DR+ T cells. Single-cell TCR profiling reveals a skewed TCRbeta repertoire enriched for TRBV11-2 and a superantigenic signature in TIM3+/CD38+/HLA-DR+ T cells. Using NicheNet, we confirm IFNgamma as a central cytokine in the communication between TIM3+/CD38+/HLA-DR+ T cells, CD16+ NK cells, and patrolling monocytes. Normalization of IFNgamma, loss of TIM3, quiescence of CD16+ NK cells, and contraction of patrolling monocytes upon clinical resolution highlight their potential role in MIS-C immunopathogenesis. Twit Text FOAVip TIM3+ TRBV11-2 T cells and IFNgamma signature in patrolling monocytes and CD16+ NK cells delineate MIS-C ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=34914824 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34914824 #FOAvip English Wikipedia <ref>{{Cite pmid|34914824}}</ref> TIM3+ TRBV11-2 T cells and IFNgamma signature in patrolling monocytes and CD16+ NK cells delineate MIS-C #MMPMID34914824 Hoste L; Roels L; Naesens L; Bosteels V; Vanhee S; Dupont S; Bosteels C; Browaeys R; Vandamme N; Verstaen K; Roels J; Van Damme KFA; Maes B; De Leeuw E; Declercq J; Aegerter H; Seys L; Smole U; De Prijck S; Vanheerswynghels M; Claes K; Debacker V; Van Isterdael G; Backers L; Claes KBM; Bastard P; Jouanguy E; Zhang SY; Mets G; Dehoorne J; Vandekerckhove K; Schelstraete P; Willems J; Stordeur P; Janssens S; Beyaert R; Saeys Y; Casanova JL; Lambrecht BN; Haerynck F; Tavernier SJ J Exp Med 2022[Feb]; 219 (2): ä PMID34914824show ga In rare instances, pediatric SARS-CoV-2 infection results in a novel immunodysregulation syndrome termed multisystem inflammatory syndrome in children (MIS-C). We compared MIS-C immunopathology with severe COVID-19 in adults. MIS-C does not result in pneumocyte damage but is associated with vascular endotheliitis and gastrointestinal epithelial injury. In MIS-C, the cytokine release syndrome is characterized by IFNgamma and not type I interferon. Persistence of patrolling monocytes differentiates MIS-C from severe COVID-19, which is dominated by HLA-DRlo classical monocytes. IFNgamma levels correlate with granzyme B production in CD16+ NK cells and TIM3 expression on CD38+/HLA-DR+ T cells. Single-cell TCR profiling reveals a skewed TCRbeta repertoire enriched for TRBV11-2 and a superantigenic signature in TIM3+/CD38+/HLA-DR+ T cells. Using NicheNet, we confirm IFNgamma as a central cytokine in the communication between TIM3+/CD38+/HLA-DR+ T cells, CD16+ NK cells, and patrolling monocytes. Normalization of IFNgamma, loss of TIM3, quiescence of CD16+ NK cells, and contraction of patrolling monocytes upon clinical resolution highlight their potential role in MIS-C immunopathogenesis. |Adolescent[MESH] |Alveolar Epithelial Cells/pathology[MESH] |B-Lymphocytes/immunology[MESH] |Blood Vessels/pathology[MESH] |COVID-19/*complications/immunology/pathology[MESH] |Cell Proliferation[MESH] |Child[MESH] |Cohort Studies[MESH] |Complement Activation[MESH] |Cytokines/metabolism[MESH] |Enterocytes/pathology[MESH] |Female[MESH] |Hepatitis A Virus Cellular Receptor 2/*metabolism[MESH] |Humans[MESH] |Immunity, Humoral[MESH] |Inflammation/pathology[MESH] |Interferon Type I/metabolism[MESH] |Interferon-gamma/*metabolism[MESH] |Interleukin-15/metabolism[MESH] |Killer Cells, Natural/*immunology[MESH] |Lymphocyte Activation/immunology[MESH] |Male[MESH] |Monocytes/*metabolism[MESH] |Receptors, Antigen, T-Cell/metabolism[MESH] |Receptors, IgG/*metabolism[MESH] |SARS-CoV-2/immunology[MESH] |Superantigens/metabolism[MESH] |Systemic Inflammatory Response Syndrome/*immunology/pathology[MESH]TIM3+ TRBV11-2 T cells and IFNgamma signature in patrolling monocytes (epmc).pdf DeepDyve Pubget Overpricing