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. 2021 Nov 15;131(22):e148225. doi: 10.1172/JCI148225

Figure 5. Increased mitochondrial content, mitochondrial ROS, and disturbed mitochondrial function in T cells from COVID-19 patients cannot be ameliorated by dexamethasone.

Figure 5

A second cohort (CII) of severe/critical COVID-19 patients receiving dexamethasone was analyzed. (A–C) Blood was drawn and processed the same day. (A) Mitochondrial content in T cells from controls and severe/critical patients of CII was analyzed beyond 19 days after intensive care unit (ICU) hospitalization and compared to cohort I (CI) and in CD4+ and CD8+ T cell subpopulations of CII. MFI, median fluorescence intensity. (B) Subset-specific expression of mitochondrial ROS in CII. (C) Citrate synthase (CS) activity, determined in T cells in which mitochondrial function was analyzed. Mitochondrial oxidative phosphorylation (OXPHOS) capacity of complex I (I) and complex I+II (I+II), capacity of the electron transfer system (I+II, ETS; after uncoupling), and ETS capacity driven by complex II (II, ETS; after rotenone administration) were determined by high-resolution respirometry. (A–C) Each symbol represents 1 donor, and summarized data are displayed as mean + SEM. *P < 0.05; **P < 0.01; ***P < 0.001 by Mann-Whitney U test (A and B subset-specific comparison).