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10.1371/journal.pone.0264979

http://scihub22266oqcxt.onion/10.1371/journal.pone.0264979
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35421120!9009616!35421120
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suck abstract from ncbi


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pmid35421120      PLoS+One 2022 ; 17 (4): e0264979
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  • Dysregulation of the leukocyte signaling landscape during acute COVID-19 #MMPMID35421120
  • Turnbull IR; Fuchs A; Remy KE; Kelly MP; Frazier EP; Ghosh S; Chang SW; Mazer MB; Hess A; Leonard JM; Hoofnagle MH; Colonna M; Hotchkiss RS
  • PLoS One 2022[]; 17 (4): e0264979 PMID35421120show ga
  • The global COVID-19 pandemic has claimed the lives of more than 750,000 US citizens. Dysregulation of the immune system underlies the pathogenesis of COVID-19, with inflammation mediated tissue injury to the lung in the setting of suppressed systemic immune function. To define the molecular mechanisms of immune dysfunction in COVID-19 we utilized a systems immunology approach centered on the circulating leukocyte phosphoproteome measured by mass cytometry. We find that although COVID-19 is associated with wholesale activation of a broad set of signaling pathways across myeloid and lymphoid cell populations, STAT3 phosphorylation predominated in both monocytes and T cells. STAT3 phosphorylation was tightly correlated with circulating IL-6 levels and high levels of phospho-STAT3 was associated with decreased markers of myeloid cell maturation/activation and decreased ex-vivo T cell IFN-gamma production, demonstrating that during COVID-19 dysregulated cellular activation is associated with suppression of immune effector cell function. Collectively, these data reconcile the systemic inflammatory response and functional immunosuppression induced by COVID-19 and suggest STAT3 signaling may be the central pathophysiologic mechanism driving immune dysfunction in COVID-19.
  • |*COVID-19[MESH]
  • |Humans[MESH]
  • |Monocytes/metabolism[MESH]
  • |Pandemics[MESH]
  • |STAT3 Transcription Factor/metabolism[MESH]
  • |Signal Transduction[MESH]


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