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10.1093/infdis/jiab425

http://scihub22266oqcxt.onion/10.1093/infdis/jiab425
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34427670!8513399!34427670
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suck abstract from ncbi


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pmid34427670      J+Infect+Dis 2021 ; 224 (10): 1672-1683
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  • Critically Ill Coronavirus Disease 2019 Patients Exhibit Hyperactive Cytokine Responses Associated With Effector Exhausted Senescent T Cells in Acute Infection #MMPMID34427670
  • Arcanjo A; Guimaraes Pinto K; Logullo J; Leite PEC; Menezes CCB; Freire-de-Lima L; Diniz-Lima I; Decote-Ricardo D; Nunes Rodrigues-da-Silva R; Geraldo Freire-de-Lima C; Almeida Filardy A; Lima-Junior JDC; Luiz Bertho A; De Luca PM; Mauro Granjeiro J; Coutinho Barroso SP; Conceicao-Silva F; Savino W; Morrot A
  • J Infect Dis 2021[Nov]; 224 (10): 1672-1683 PMID34427670show ga
  • BACKGROUND: Coronavirus disease 2019 (COVID-19) can progress to severe pneumonia with respiratory failure and is aggravated by the deregulation of the immune system causing an excessive inflammation including the cytokine storm. METHODS: In this study, we report that severe acutely infected patients have high levels of both type-1 and type-2 cytokines. RESULTS: Our results show abnormal cytokine levels upon T-cell stimulation, in a nonpolarized profile. Furthermore, our findings indicate that this hyperactive cytokine response is associated with a significantly increased frequency of late-differentiated T cells with particular phenotype of effector exhausted/senescent CD28-CD57+ cells. Of note, we demonstrated for the first time an increased frequency of CD3+CD4+CD28-CD57+ T cells with expression of programmed death 1, one of the hallmarks of T-cell exhaustion. CONCLUSIONS: These findings reveal that COVID-19 is associated with acute immunodeficiency, especially within the CD4+ T-cell compartment, and points to possible mechanisms of loss of clonal repertoire and susceptibility to viral relapse and reinfection events.
  • |*COVID-19[MESH]
  • |CD28 Antigens[MESH]
  • |Critical Illness[MESH]
  • |Cytokines/metabolism[MESH]
  • |Humans[MESH]


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