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Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection

Perez-Gomez, A.; Vitalle, J.; Gasca-Capote, M. d. C.; Gutierrez-Valencia, A.; Trujillo-Rodriguez, M.; Serna-Gallego, A.; Munoz-Muela, E.; Jimenez-Leon, M. d. l. R.; Rafii-El-Idrissi Benhnia, M.; Rivas-Jeremias, I.; Sotomayor, C.; Roca-Oporto, C.; Espinosa, N.; Infante-Dominguez, C.; Crespo-Rivas, J. C.; Fernandez-Villar, A.; Perez-Gonzalez, A.; Lopez-Cortes, L. F.; Poveda, E.; Ruiz-Mateos, E.

2021-03-19 immunology
10.1101/2021.03.18.436001 bioRxiv
Show abstract

Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components. Dendritic cells (DCs) play a key role in the defense against viral infections, for instance plasmacytoid DCs (pDCs), have the capacity to produce vast amounts of interferon-alpha (IFN-). In COVID-19 there is a deficit in DC numbers and IFN- production, which has been associated with disease severity. In this work, we described that in addition to the DC deficiency, several DC activation and homing markers were altered in acute COVID-19 patients, which were associated with multiple inflammatory markers. Remarkably, previously hospitalized and non-hospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection. Moreover, the expression of DC markers as CD86 and CD4 were only restored in previously non-hospitalized patients while integrin {beta}7 and indoleamine 2,3- dyoxigenase (IDO) no restoration was observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19.

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