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

Pérez-Gómez, Alberto; Vitallé, Joana; Gasca-Capote, Carmen; Gutierrez-Valencia, Alicia; Trujillo-Rodriguez, María; Serna-Gallego, Ana; Muñoz-Muela, Esperanza; Jiménez-Leon, María de los Reyes; Rafii-El-Idrissi Benhnia, Mohamed; Rivas-Jeremias, Inmaculada; Sotomayor, Cesar; Roca-Oporto, Cristina; Espinosa, Nuria; Infante-Domínguez, Carmen; Crespo-Rivas, Juan Carlos; Fernández-Villar, Alberto; Pérez-González, Alexandre; López-Cortés, Luis Fernando; Poveda, Eva; Ruiz-Mateos, Ezequiel

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.