Fatty acid oxidation is the main source of elevated OXPHOS in IL-10 stimulated NK cells. Ex vivo expanded and freshly-isolated NK cells were treated with IL-10 for 16 h. (A–C) Real-time analyses of OCR in IL-10 stimulated ex vivo expanded NK cells with inhibition of fatty acid oxidation (A), pyruvate transportation (B), or glutaminolysis (C). OCR was measured at baseline followed by the addition of medium (red) or etomoxir (Eto, 150 μM, blue, A) or UK5099 (10 μM, green, B), or BPTES (5 μM, purple, C) and the sequential injection of oligomycin, FCCP, and rotenone plus antimycin (R&A). (D–F) Quantification of basal respiration, ATP-linked respiration and maximal respiration of IL-10 stimulated ex vivo expanded NK cells with inhibition of fatty acid oxidation (D), pyruvate transportation (E), or glutaminolysis (F). (G–I) Real-time analyses of OCR of IL-10 stimulated freshly-isolated NK cells with inhibition of fatty acid oxidation (G), pyruvate import (H), or glutaminolysis (I). OCR was measured as described in (A–C). (J–L) Quantification of basal respiration, ATP-linked respiration and maximal respiration of IL-10 stimulated freshly-isolated NK cells with inhibition of fatty acid oxidation (J), pyruvate transportation (K), or glutaminolysis (L). The results were presented as Mean ± SEM [n = 4-5 for (A–F), n = 3–6 for (G–L)]. Data were compared using independent Student's t-test. *P < 0.05; **P < 0.01; ***P < 0.001.