Hobit and Blimp1 instruct a universal transcriptional program of tissue residency in lymphocytes
- Author(s)
- Mackay, LK; Minnich, M; Kragten, NA; Liao, Y; Nota, B; Seillet, C; Zaid, A; Man, K; Preston, S; Freestone, D; Braun, A; Wynne-Jones, E; Behr, FM; Stark, R; Pellicci, DG; Godfrey, DI; Belz, GT; Pellegrini, M; Gebhardt, T; Busslinger, M; Shi, W; Carbone, FR; van Lier, RA; Kallies, A; van Gisbergen, KP;
- Details
- Publication Year 2016-04-22,Volume 352,Issue #6284,Page 459-63
- Journal Title
- Science
- Publication Type
- Journal Article
- Abstract
- 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.
- Publisher
- AAAS
- Research Division(s)
- Molecular Immunology; Infection And Immunity; Bioinformatics
- PubMed ID
- 27102484
- Publisher's Version
- https://doi.org/10.1126/science.aad2035
- NHMRC Grants
- NHMRC/1042582, NHMRC/637345,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2016-05-02 10:21:21
Last Modified: 2016-05-05 11:31:17