Pérez-Gómez, AlbertoVitallé, JoanaGasca-Capote, CarmenGutierrez-Valencia, AliciaTrujillo-Rodriguez, MaríaSerna-Gallego, AnaMuñoz-Muela, EsperanzaJiménez-Leon, María de Los ReyesRafii-El-Idrissi Benhnia, MohamedRivas-Jeremias, InmaculadaSotomayor, CesarRoca-Oporto, CristinaEspinosa, NuriaInfante-Domínguez, CarmenCrespo-Rivas, Juan CarlosFernández-Villar, AlbertoPérez-González, AlexandreLópez-Cortés, Luis FernandoPoveda, EvaRuiz-Mateos, EzequielVirgen del Rocío Hospital COVID-19 Working Team2023-02-092023-02-092021-07-21http://hdl.handle.net/10668/18233Severe 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.enCOVID-19Dendritic cellLong-COVIDSARS-CoV-2COVID-19Cells, CulturedDendritic CellsFemaleHumansImmunity, InnateInflammationInterferon-alphaLeukocytes, MononuclearMaleSARS-CoV-2Severity of Illness Indexresearch article34290398open access10.1038/s41423-021-00728-22042-0226PMC8294321https://www.nature.com/articles/s41423-021-00728-2.pdfhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8294321/pdf