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10.4049/jimmunol.2001034

http://scihub22266oqcxt.onion/10.4049/jimmunol.2001034
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33558375!ä!33558375

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suck abstract from ncbi


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pmid33558375      J+Immunol 2021 ; 206 (7): 1478-1482
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  • T Cell Phenotyping in Individuals Hospitalized with COVID-19 #MMPMID33558375
  • Rupp J; Dreo B; Gutl K; Fessler J; Moser A; Haditsch B; Schilcher G; Matzkies LM; Steinmetz I; Greinix H; Stradner MH
  • J Immunol 2021[Apr]; 206 (7): 1478-1482 PMID33558375show ga
  • Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has become pandemic. Cytokine release syndrome occurring in a minority of SARS-CoV-2 infections is associated with severe disease and high mortality. We profiled the composition, activation, and proliferation of T cells in 20 patients with severe or critical COVID-19 and 40 matched healthy controls by flow cytometry. Unsupervised hierarchical cluster analysis based on 18 T cell subsets resulted in separation of healthy controls and COVID-19 patients. Compared to healthy controls, patients suffering from severe and critical COVID-19 had increased frequencies of activated and proliferating CD38(+)Ki67(+) CD4(+) and CD8(+) T cells, suggesting active antiviral T cell defense. Frequencies of CD38(+)Ki67(+) Th1 and CD4(+) cells correlated negatively with plasma IL-6. Thus, our data suggest that patients suffering from COVID-19 have a distinct T cell composition that is potentially modulated by IL-6.
  • |*Immunity, Cellular[MESH]
  • |ADP-ribosyl Cyclase 1/immunology[MESH]
  • |Adult[MESH]
  • |CD8-Positive T-Lymphocytes/*immunology/pathology[MESH]
  • |COVID-19/epidemiology/*immunology/pathology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Immunophenotyping[MESH]
  • |Interleukin-6/immunology[MESH]
  • |Ki-67 Antigen/immunology[MESH]
  • |Male[MESH]
  • |Membrane Glycoproteins/immunology[MESH]
  • |Pandemics[MESH]
  • |Retrospective Studies[MESH]
  • |SARS-CoV-2/*immunology[MESH]


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