Extended Data Fig. 3: Response of TOX-deficient T cells in acute and chronic LCMV.

a, The gating strategy used in co-adoptive transfer and infection experiments. b, Expression of activation markers and transcription factors in naive wild-type and Tox^flox/floxCd4^cre P14 T cells before adoptive transfer. Wild-type and TOX cKO T cells were mixed 1:1 and adoptively transferred into congenic wild-type mice followed by infection with Armstrong (c, d, f–k) or clone 13 (c–e). c, Frequency of wild-type or TOX cKO P14 T cells during infection with Armstrong or clone 13. d, TOX expression in wild-type and TOX cKO P14 T cells after infection with Armstrong or clone 13. e, Ki-67 expression on day 8 of clone-13 infection. f, g, Frequency of memory populations on day 8 (f) or day 30 (g) of Armstrong infection. h, Transcription-factor expression in wild-type and TOX cKO P14 T cells on day 30 post-infection with Armstrong. i–k, Cytokine and effector molecule (i), inhibitory-receptor (j), and transcription-factor (k) expression on day 8 post-infection with Armstrong. Inhibitory-receptor expression is reported as the ratio of the median fluorescent intensity between TOX cKO and wild-type P14 T cells (j, right). l, GSEA of transcriptional signatures associated with naive T or T_mem cells compared to the differentially expressed genes in Tox^−/− versus wild-type P14 T cells. m, Expression of genes associated with the terminal short-lived subset of T_eff cells²⁶. n, Comparison of the transcriptional signature of TOX cKO and TCF-1 cKO³⁰ T cells after 8 days of clone-13 infection. Genes differentially expressed relative to wild-type (FDR < 0.05 and log-fold change > 0.6) were compared between datasets. Contour and histogram plots are representative of at least 4 independent experiments with at least 4 mice. Statistical significance (*P < 0.01) was determined by a pairwise t-test with Holm–Sidak correction (c) or the Student’s t-test (e–l), error is reported as s.d.