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10.1111/bjh.18062

http://scihub22266oqcxt.onion/10.1111/bjh.18062
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35076084!ä!35076084

suck abstract from ncbi


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pmid35076084      Br+J+Haematol 2022 ; 197 (3): 283-292
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  • Platelets modulate CD4(+) T-cell function in COVID-19 through a PD-L1 dependent mechanism #MMPMID35076084
  • Paletta A; Di Diego Garcia F; Varese A; Erra Diaz F; Garcia J; Cisneros JC; Luduena G; Mazzitelli I; Pisarevsky A; Cabrerizo G; Lopez Malizia A; Rodriguez AG; Lista N; Longueira Y; Sabatte J; Geffner J; Remes Lenicov F; Ceballos A
  • Br J Haematol 2022[May]; 197 (3): 283-292 PMID35076084show ga
  • Severe COVID-19 is associated with a systemic inflammatory response and progressive CD4(+) T-cell lymphopenia and dysfunction. We evaluated whether platelets might contribute to CD4(+) T-cell dysfunction in COVID-19. We observed a high frequency of CD4(+) T cell-platelet aggregates in COVID-19 inpatients that inversely correlated with lymphocyte counts. Platelets from COVID-19 inpatients but not from healthy donors (HD) inhibited the upregulation of CD25 expression and tumour necrosis factor (TNF)-alpha production by CD4(+) T cells. In addition, interferon (IFN)-gamma production was increased by platelets from HD but not from COVID-19 inpatients. A high expression of PD-L1 was found in platelets from COVID-19 patients to be inversely correlated with IFN-gamma production by activated CD4(+) T cells cocultured with platelets. We also found that a PD-L1-blocking antibody significantly restored platelets' ability to stimulate IFN-gamma production by CD4(+) T cells. Our study suggests that platelets might contribute to disease progression in COVID-19 not only by promoting thrombotic and inflammatory events, but also by affecting CD4(+) T cells functionality.
  • |*B7-H1 Antigen/metabolism[MESH]
  • |*COVID-19[MESH]
  • |Blood Platelets/metabolism[MESH]
  • |CD4-Positive T-Lymphocytes[MESH]
  • |Humans[MESH]


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