Platelets modulate CD4 + T-cell function in COVID-19 through a PD-L1 dependent mechanism.

Autor: Paletta A; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Di Diego García F; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Varese A; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Erra Diaz F; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., García J; División C, Hospital de Enfermedades Infecciosas Francisco Muñiz, Buenos Aires, Argentina., Cisneros JC; Unidad de Terapia Intensiva, Hospital de Enfermedades Infecciosas Francisco Muñiz, Buenos Aires, Argentina., Ludueña G; Departamento de Medicina Interna, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina., Mazzitelli I; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Pisarevsky A; Departamento de Medicina Interna, Hospital de Clínicas, Universidad de Buenos Aires, Buenos Aires, Argentina., Cabrerizo G; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., López Malizia Á; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Rodriguez AG; Unidad de Terapia Intensiva, Hospital de Enfermedades Infecciosas Francisco Muñiz, Buenos Aires, Argentina., Lista N; Unidad de Terapia Intensiva, Hospital de Enfermedades Infecciosas Francisco Muñiz, Buenos Aires, Argentina., Longueira Y; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Sabatté J; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Geffner J; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Remes Lenicov F; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina., Ceballos A; Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Universidad de Buenos Aires (UBA)-CONICET, Buenos Aires, Argentina.
Jazyk: angličtina
Zdroj: British journal of haematology [Br J Haematol] 2022 May; Vol. 197 (3), pp. 283-292. Date of Electronic Publication: 2022 Feb 16.
DOI: 10.1111/bjh.18062
Abstrakt: 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)-α production by CD4 + T cells. In addition, interferon (IFN)-γ 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-γ 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-γ 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.
(© 2022 British Society for Haematology and John Wiley & Sons Ltd.)
Databáze: MEDLINE
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