Memory CD4+ T-Cell Lymphocytic Angiopathy in Fatal Forms of COVID-19 Pulmonary Infection

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Guihot, Amélie | Plu, Isabelle | Soulié, Cathia | Rousseau, Alice | Nakid-Cordero, Cecilia | Dorgham, Karim | Parizot, Christophe | Litvinova, Elena | Mayaux, Julien | Malet, Isabelle | Quentric, Paul | Combadière, Béhazine | Combadière, Christophe | Bonduelle, Olivia | Adam, Lucille | Rosenbaum, Pierre | Beurton, Alexandra | Hémon, Patrice | Debré, Patrice | Vieillard, Vincent | Autran, Brigitte | Seilhean, Danielle | Charlotte, Frédéric | Marcelin, Anne-Geneviève | Gorochov, Guy | Luyt, Charles-Edouard

Edité par CCSD ; Frontiers -

International audience. The immunopathological pulmonary mechanisms leading to Coronavirus Disease (COVID-19)-related death in adults remain poorly understood. Bronchoalveolar lavage (BAL) and peripheral blood sampling were performed in 74 steroid and non-steroid-treated intensive care unit (ICU) patients (23–75 years; 44 survivors). Peripheral effector SARS-CoV-2-specific T cells were detected in 34/58 cases, mainly directed against the S1 portion of the spike protein. The BAL lymphocytosis consisted of T cells, while the mean CD4/CD8 ratio was 1.80 in non-steroid- treated patients and 1.14 in steroid-treated patients. Moreover, strong BAL SARS-CoV-2 specific T-cell responses were detected in 4/4 surviving and 3/3 non-surviving patients. Serum IFN-γ and IL-6 levels were decreased in steroid-treated patients when compared to non-steroid treated patients. In the lung samples from 3 (1 non-ICU and 2 ICU) additional deceased cases, a lymphocytic memory CD4 T-cell angiopathy colocalizing with SARS-CoV-2 was also observed. Taken together, these data show that disease severity occurs despite strong antiviral CD4 T cell-specific responses migrating to the lung, which could suggest a pathogenic role for perivascular memory CD4 T cells upon fatal COVID-19 pneumonia.

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