| Literature DB >> 27102484 |
Laura K Mackay1, Martina Minnich2, Natasja A M Kragten3, Yang Liao4, Benjamin Nota5, Cyril Seillet4, Ali Zaid6, Kevin Man4, Simon Preston4, David Freestone6, Asolina Braun6, Erica Wynne-Jones6, Felix M Behr7, Regina Stark3, Daniel G Pellicci8, Dale I Godfrey8, Gabrielle T Belz4, Marc Pellegrini4, Thomas Gebhardt6, Meinrad Busslinger2, Wei Shi9, Francis R Carbone6, René A W van Lier3, Axel Kallies10, Klaas P J M van Gisbergen11.
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.Entities:
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Year: 2016 PMID： 27102484 DOI： 10.1126/science.aad2035
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728