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The article discusses three reports within the issue on immunology research, including one by N. Iijima and A. Iwasaki, one by J. M. Schenkel et al., and one by S. Ariotti et al., investigating the molecular mechanisms underlying the persistence and protective function of tissue-resident memory T cells (TRM). Topics include CD4 TRM cell retention, TRM cell activation, and infection control involving the cytokine interferon-γ (IFN-γ).

Tissue-resident memory T (Trm) cells permanently localize to portals of pathogen entry, where they provide immediate protection against reinfection.To enforce tissue retention, Trm cells up-regulate CD69 and down-regulate molecules associated with tissue egress; however, a Trm-specific transcriptional regulator has not been identified. Here, we show that the transcription factor Hobit is specifically up-regulated in Trm cells and, together with related Blimp1, mediates the development of Trm cells in skin, gut, liver, and kidney in mice. The Hobit-Blimp1 transcriptional module is also required for other populations of tissue-resident lymphocytes, including natural killer T (NKT) cells and liver-resident NK cells, all of which share a common transcriptional program. Our results identify Hobit and Blimp1 as central regulators of this universal program that instructs tissue retention in diverse tissue-resident lymphocyte populations. [ABSTRACT FROM AUTHOR]