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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Clin+Invest 2020 ; 130 (12): 6290-6300 Nephropedia Template TP
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COVID-19 severity associates with pulmonary redistribution of CD1c+ DCs and inflammatory transitional and nonclassical monocytes #MMPMID32784290
Sanchez-Cerrillo I; Landete P; Aldave B; Sanchez-Alonso S; Sanchez-Azofra A; Marcos-Jimenez A; Avalos E; Alcaraz-Serna A; de Los Santos I; Mateu-Albero T; Esparcia L; Lopez-Sanz C; Martinez-Fleta P; Gabrie L; Del Campo Guerola L; de la Fuente H; Calzada MJ; Gonzalez-Alvaro I; Alfranca A; Sanchez-Madrid F; Munoz-Calleja C; Soriano JB; Ancochea J; Martin-Gayo E
J Clin Invest 2020[Dec]; 130 (12): 6290-6300 PMID32784290show ga
SARS-CoV-2 is responsible for the development of coronavirus disease 2019 (COVID-19) in infected individuals, who can either exhibit mild symptoms or progress toward a life-threatening acute respiratory distress syndrome (ARDS). Exacerbated inflammation and dysregulated immune responses involving T and myeloid cells occur in COVID-19 patients with severe clinical progression. However, the differential contribution of specific subsets of dendritic cells and monocytes to ARDS is still poorly understood. In addition, the role of CD8+ T cells present in the lung of COVID-19 patients and relevant for viral control has not been characterized. Here, we have studied the frequencies and activation profiles of dendritic cells and monocytes present in the blood and lung of COVID-19 patients with different clinical severity in comparison with healthy individuals. Furthermore, these subpopulations and their association with antiviral effector CD8+ T cell subsets were also characterized in lung infiltrates from critical COVID-19 patients. Our results indicate that inflammatory transitional and nonclassical monocytes and CD1c+ conventional dendritic cells preferentially migrate from blood to lungs in patients with severe COVID-19. Thus, this study increases the knowledge of specific myeloid subsets involved in the pathogenesis of COVID-19 disease and could be useful for the design of therapeutic strategies for fighting SARS-CoV-2 infection.