Fig. 3.

T cell–intrinsic IL-27 signaling mediates control of persistent LCMV infection. IL-27ra^flox/flox (WT) and CD4-Cre/IL-27ra^flox/flox mice (T cell–specific IL-27ra KO) were infected with 2 × 10⁶ PFU LCMV Cl-13. (A) Serum viral loads were determined throughout infection. (B–F) At day 120 p.i., viral loads were measured in (B) lung, (C) spleen, (D) kidney, (E) brain, and (F) liver. (G–J) At day 9 p.i., splenocytes were analyzed by flow cytometry to determine the total number of (G) H2-Db GP_33–41 virus-specific CD8 T cells, (H) IFN-γ–producing GP_33–41 LCMV-specific CD8 T cells, (I) polyfunctional IFN-γ– and TNF-α–producing GP_33–41 LCMV-specific CD8 T cells, and (J) IFN-γ–producing GP_61–80 LCMV-specific CD4 T cells. (K–N) At day 40 p.i., splenocytes were analyzed by flow cytometry to determine the number of (K) I-Ab GP_67–77⁺ CD4 T cells, (L) IFN-γ⁺–producing CD4 T cells after GP_67–80 peptide stimulation, (M) Tfh cells, and (N) IL-21⁺IFN-γ⁺ Tfh cells after PMA and ionomycin stimulation. Data are representative of three experimental replicates and error bars represent mean ± SD from 4 to 10 mice per group. Statistical analyses of experimental groups were performed using the Mann–Whitney U test (A–F) or Student’s two-tailed t test (G–N); not significant (ns), P > 0.05; *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001.