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

AuthorsPérez-Gómez, Alberto; Vitallé, Joana; Gasca-Capote, María del Carmen; Gutiérrez Valencia, Alicia; Trujillo-Rodríguez, María; Serna, Ana CSIC ORCID; Muñoz-Muela, Esperanza; Jiménez-León, María Reyes; Rafii-El-Idrissi Benhnia, Mohamed; Rivas-Jeremias, Inmaculada; Sotomayor, César; Roca-Oporto, Cristina; Espinosa, Nuria; Infante-Domínguez, Carmen; Crespo-Rivas, Juan Carlos; Fernández-Villar, Alberto; Pérez-González, Alexandre; López-Cortés, Luis F. CSIC; Poveda, Eva; Ruiz-Mateos, Ezequiel
Dendritic cells
Integrin β7
Lack of recovery
Issue Date19-Mar-2021
CitationBioRxiv: 10.1101/2021.03.18.436001 (2021)
AbstractSevere 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 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 β7 and indoleamine 2,3-dyoxigenase (IDO) no restoration was observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19.
Publisher version (URL)https://doi.org/10.1101/2021.03.18.436001
Appears in Collections:(IBIS) Artículos
(VICYT) Colección Especial COVID-19
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