RT Journal Article
T1 Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection.
A1 Pérez-Gómez, Alberto
A1 Vitallé, Joana
A1 Gasca-Capote, Carmen
A1 Gutierrez-Valencia, Alicia
A1 Trujillo-Rodriguez, María
A1 Serna-Gallego, Ana
A1 Muñoz-Muela, Esperanza
A1 Jiménez-Leon, María de Los Reyes
A1 Rafii-El-Idrissi Benhnia, Mohamed
A1 Rivas-Jeremias, Inmaculada
A1 Sotomayor, Cesar
A1 Roca-Oporto, Cristina
A1 Espinosa, Nuria
A1 Infante-Domínguez, Carmen
A1 Crespo-Rivas, Juan Carlos
A1 Fernández-Villar, Alberto
A1 Pérez-González, Alexandre
A1 López-Cortés, Luis Fernando
A1 Poveda, Eva
A1 Ruiz-Mateos, Ezequiel
A1 Virgen del Rocío Hospital COVID-19 Working Team, 
K1 COVID-19
K1 Dendritic cell
K1 Long-COVID
K1 SARS-CoV-2
AB 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-α). In COVID-19 there is a deficit in DC numbers and IFN-α 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 nonhospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection. Moreover, the expression of DC markers such as CD86 and CD4 were only restored in previously nonhospitalized patients, while no restoration of integrin β7 and indoleamine 2,3-dyoxigenase (IDO) levels were observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19.
YR 2021
FD 2021-07-21
LK http://hdl.handle.net/10668/18233
UL http://hdl.handle.net/10668/18233
LA en
DS RISalud
RD Apr 14, 2025