Journal
SCIENCE
Volume 352, Issue 6284, Pages 459-463Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad2035
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Funding
- ARC [DE140100432]
- National Health and Medical Research Council of Australia (NHMRC) [1083685]
- Boehringer Ingelheim
- European Research Council from the European Community [291740-LymphoControl]
- German Research Foundation
- Alexander von Humboldt Foundation
- NHMRC [1023454, 1054431, 1020770, 1042582, 637345]
- Landsteiner Foundation of Blood Transfusion Research [1136]
- ARC
- Sylvia and Charles Viertel Foundation
- Vidi from The Netherlands Organization of Scientific Research [917.13.338]
- Victorian State Government
- Australian Government NHMRC Independent Research Institute Infrastructure Support scheme
- National Health and Medical Research Council of Australia [1083685] Funding Source: NHMRC
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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.
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