Extended Data Fig. 7: Efficient depletion of T_RM cells by DT administration.

Wild-type mice containing congenically marked naïve WT and HR OT-I T cells were infected orally with L.m.-OVA. DT was administered in the memory phase after infection to specifically deplete HR T_RM cells. One day after the last DT administration, presence and phenotype of donor WT and HR OT-I T cells were analyzed. a, Representative flow cytometry plots show expression of CD8α and tdTomato by HR OT-I T cells in liver under control conditions (left) and after DT treatment (right). b, Hobit⁺ HR OT-I cells were enumerated in control (Ctrl) and DT-treated mice. Two-tailed unpaired t-test, **P = 0.0023, ***P = 0.0007. (c–i) The contribution of WT and HR OT-I T cells to the formation of primary memory populations was analyzed in control and DT-treated mice. (c–f) Representative flow cytometry plots show expression of CD45.1 and CD45.2 to identify the presence of WT (CD45.1⁺) and HR (CD45.2⁺) OT-I T cells within (c) CD69⁺ T_RM cells in liver, (d) CD69⁺ T_RM cells in SI IEL, (e) CD62L⁺ T_CM cells in spleen, and (f) KLRG1⁺ T_EM cells in spleen under control conditions (left) and after DT-treatment (right). (g–i) The ratio between HR and WT OT-I T cells was determined under control conditions and after DT treatment for (g) the CD69⁺ T_RM population of liver and SI IEL, (h) the CD62L⁺ T_CM population of spleen and mLN, and (i) the KLRG1⁺ T_EM population of spleen and liver. Ratios were normalized to controls. Two-tailed Mann-Whitney U-test, *P = 0.0286. Data from one experiment (n = 4 mice). Symbols represent individual mice; bars represent the mean.