Impaired function and delayed regeneration of dendritic cells in COVID-19
Winheim, E.; Rinke, L.; Lutz, K.; Reischer, A.; Leutbecher, A.; Wolfram, L.; Rausch, L.; Kranich, J.; Wratil, P. R.; Huber, J.; Baumjohann, D.; Rothenfusser, S.; Hellmuth, J.; Scherer, C.; Muenchhoff, M.; von Bergwelt-Baildon, M.; Stark, K.; Straub, T.; Brocker, T.; Keppler, O. T.; Subklewe, M.; Krug, A. B.
Show abstract
Disease manifestations in COVID-19 range from mild to severe illness associated with a dysregulated innate immune response. Alterations in function and regeneration of dendritic cells (DC) and monocytes may contribute to immunopathology and influence adaptive immune responses in COVID-19 patients. We analyzed circulating DC and monocyte subsets in 65 hospitalized COVID-19 patients with mild/moderate or severe disease from acute disease to recovery and in healthy controls. Persisting reduction of all DC subpopulations was accompanied by an expansion of proliferating Lineage- HLADR+ cells lacking DC markers. Increased frequency of the recently discovered CD163+ CD14+ DC3 subpopulation in patients with more severe disease was associated with systemic inflammation, activated T follicular helper cells, and antibody-secreting cells. Persistent downregulation of CD86 and upregulation of PD-L1 in conventional DC (cDC2 and DC3) and classical monocytes associated with a reduced capacity to stimulate naive CD4+ T cells correlated with disease severity. Long-lasting depletion and functional impairment of DCs and monocytes may have consequences for susceptibility to secondary infections and therapy of COVID-19 patients.
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