Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. Persistent TCR–pMHC-I signaling drives the formation.

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Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. H2dbfl/fl (Ctl) and H2dbΔUbc-creERT2 (KO) mice were infected with influenza PR8 and then treated with tamoxifen starting at 22 d.p.i. Spleens and lungs were harvested after intravenous administration of CD45 Ab at 42 d.p.i. (A) Schematic of the experimental design. (B) Average PD-1 or TIM-3 expression levels (MFI) on NP366–374 TRM cells evaluated by flow cytometry. (C) Average PD-1 or TIM-3 expression levels (MFI) on PA224–233 TRM cells evaluated by flow cytometry. (D) Representative plots and average frequencies of TRM cells (top) or TM-SPL cells (bottom) in lung-resident or splenic CD8+ T cells, respectively. (E) Cell numbers of NP366–374 or PA224–233 TRM cells. (F) Representative plot of CD103 expression on NP366–374 TRM cells. (G) Average CD103 expression levels (MFI) on NP366–374 or PA224–233 TRM cells were evaluated by flow cytometry. Representative of three experiments (n = 4 mice per group). Data are mean ± SD; ns, not significant. *P < 0.05, **P < 0.01, unpaired two-tailed t test. Zheng Wang et al. Sci. Immunol. 2019;4:eaaw1217 Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works