Fig. 2 |. OPA1 deficiency in IL-17A-expressing cells ameliorates T_H17-mediated autoimmune pathogenesis.

a, Immunoblot of CD4⁺TCRβ⁺ cells expressing enhanced yellow fluorescent protein (eYFP) (T_H17 cells) isolated from control and Opa1^Il17a-cre reporter mice. Actin is used as a loading control. b, Surface markers on CD4⁺TCRβ⁺eYFP⁺ cells and CD4⁺ T_N cells (CD4⁺CD44^lowCD62L^high) from small intestine lamina propria. c, Frequency of live CD4⁺TCRβ⁺eYFP⁺ cells in the small intestine lamina propria (LP) (control: n = 10, Opa1^Il17a-cre: n = 10 mice), Peyer’s patches (PPs) (control: n = 7, Opa1^Il17a-cre: n = 10 mice) and MLN (control: n = 8, Opa1^Il17a-cre: n = 10 mice), 2 independent experiments. d,e, Mice were injected with anti-CD3 antibody every 48 h for 100 h. Frequency of CD4⁺TCRβ⁺eYFP⁺ cells (n = 5 mice) (d) and IL-17A expression in restimulated CD4⁺TCRβ⁺eYFP⁺ cells (e) (control: n = 7, Opa1^Il17a-cre: n = 8 mice, 2 independent experiments). f, Mice were immunized with myelin oligodendrocyte glycoprotein (MOG) peptide and monitored for clinical disease score (n = 7 mice per group). g, Frequency of CD4⁺TCRβ⁺eYFP⁺ cells from brain, spinal cord (SC) and draining lymph nodes (dLNs) 20 days after immunization (n = 8 mice per genotype, 2 independent experiments). h, Expression of IL-17A and IFNγ in brain CD4⁺TCRβ⁺eYFP⁺ cells (control: n = 13, Opa1^Il17a-cre: n = 9 mice, 2 independent experiments). i–k, Expression of RORγt and TBET (i; n = 6 mice per genotype), Ki67 (j) and active caspase-3 (k) (n= 8 mice per genotype, 2 independent experiments) in CD4⁺TCRβ⁺eYFP⁺ cells from brain (i) and spinal cord (j ,k). Representative plots and graphs summarize results of at least two independent experiments, except where noted otherwise. Data are mean ± s.e.m. Two-sided šidák’s test (c,f‘h) or unpaired two-tailed t-test (d,e,i‘k). Exact P-values are indicated.