Extended Data Fig. 6: Effect of ABHD11 inhibition on CD8+ T cell metabolism.
From: Lipoyl deglutarylation by ABHD11 regulates mitochondrial and T cell metabolism
a–c, Human CD8+ T cells were isolated from healthy donor peripheral blood mononuclear cells, activated with anti-CD3/CD28 Dynabeads and continuously treated with 1 µM ML226 for 11 days. Cell numbers were quantified at 4, 7 and 11 days, and normalized to the vehicle control for each time point. Each data point represents one donor. Mean ± s.e.m.; n = 6 donors; two-way ANOVA and Dunnett’s post-hoc test. b,c, Oxygen consumption rate (OCR) after 11 days during a mitochondrial stress test (1 μM oligomycin, 1.5 μM FCCP, 100 nM rotenone + 1 μM antimycin) was quantified using a Seahorse XFe96 Extracellular Flux Analyzer (b). Mean ± s.e.m.; n = 6 donors. Quantification of basal OCR, ATP production, maximal respiration and nonmitochondrial respiration (c). Each data point represents one donor. Mean ± s.d.; n = 6 donors; unpaired two-tailed t-test. d, Activated CD8+ T cells were cultured for 10 days and treated with 1 µM ML226 for 24 h. OCR during a mitochondrial stress test (1 μM oligomycin, 1.5 μM FCCP, 100 nM rotenone + 1 μM antimycin). Mean ± s.e.m.; n = 4 donors. e,f, Activated human CD8+ T cells were continuously treated with 1 µM ML226 for 11 days. Extracellular acidification (ECAR) during a mitochondrial stress test (e). Mean ± s.e.m.; n = 6 donors. Quantification of basal ECAR (f). Each data point represents one donor. Mean ± s.d.; n = 6 donors; unpaired two-tailed t-test.
