Loss of Xcl1 expression leads to defective T _RM formation during acute viral infection. (A) scRNA-seq expression of Xcl1 in P14 T cells during LCMV-Arm timecourse (data from Kurd et al. [2020]). (B) Experiment setup in which P14 T cells were electroporated with a control (sgThy1) or experimental (sgXcl1) ribonucleoprotein complex. P14 T cells were transferred into congenically distinct mice prior to LCMV-Arm infection. Tissues isolated at effector (D8) and memory (D25) time points. (C) Quantification of P14 frequency at D8 (left), CCR9 frequency at D8 (right). (D) Circulating P14 T cell frequency and number D25 after infection. (E) Representative plots of CD69 and CD103 in indicated tissues at D25 after infection (left). Quantification of frequency and absolute number (right). (F) Quantification of P14 T cell number D25 after infection. (G) Concatenated histogram of P2RX7 expression across sgThy1 control P14 T cell IEL subsets at D25 (top). Quantification of frequency and number of IEL CD69⁺ P2RX7⁺ cells at D25 (bottom). P14 T cells gated on CD8α (IV⁻) on all tissues except the spleen. Data are pooled from two independent experiments, n = 8 (sgThy1) and n = 7 (sgXcl1). P values shown, n.s. = not significant. Two-way ANOVA (C, D, and F) and unpaired t test (E and G).