Figure 2. Memory T cell development and survival, unlike effectors, requires mitochondrial fusion.

(A) Relative in vitro survival ratios of Mfn1, Mfn2, or Opa1 deficient (CD4 Cre⁺, −/−) to wild-type (CD4 Cre^-, +/+) OT-I IL-2 T_E and IL-15 T_M cells (*p=0.0465). Data normalized from 2–3 independent experiments shown as mean ± SEM. (B) Mitochondrial morphology of OT-I Opa1 wild-type and Opa1^−/− IL-2 T_E and IL-15 T_M cells analyzed by EM (scale bar = 0.5 µm, represents one experiment) and (C) Seahorse EFA. (Left) bar graph represents ratios of O₂ consumption rates (OCR, indicator of OXPHOS) to extracellular acidification rates (ECAR, indicator of aerobic glycolysis) at baseline and (right) spare respiratory capacity (SRC) (% max OCR after FCCP injection of baseline OCR) of indicated cells (*p<0.03, **p=0.0079). Data from 3 experiments shown as mean ± SEM. (D–F) 10⁴ OT-I Opa1^+/+ or Opa1^−/− T cells were transferred i.v. into C57BL/6 CD90.1 mice infected i.v. with 10⁷ CFU LmOVA. Blood analyzed by flow cytometry at indicated times post infection. After 21 days, mice were challenged i.v. with 5×10⁷ CFU LmOVA and blood analyzed post challenge (p.c.). (D) % Donor K^b/OVA⁺ CD90.2⁺ cells shown in representative flow plots and (E) line graph with mean ± SEM (*p=0.0238, **p<0.005). (F) Number of donor K^b/OVA⁺ cells from spleens of infected mice shown with mean ± SEM (*p=0.0126). (D–F) Representative of 2 experiments (n=9–11/ group). See also Figure S2.