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We have previously shown that the transcription factor Hobit and its homolog Blimp\u20101 drive Trm development after viral infection, but how and when these transcription factors mediate Trm formation remains poorly understood. In particular, the major impact of Blimp\u20101 in regulating several aspects of effector T\u2010cell differentiation impairs study of its specific role in Trm development. Here, we used the restricted expression of Hobit in the Trm lineage to develop mice with a conditional deletion of Blimp\u20101 in Trm, allowing us to specifically investigate the role of both transcription factors in Trm differentiation. We found that Hobit and Blimp\u20101 were required for the upregulation of CD69 and suppression of CCR7 and S1PR1 on virus\u2010specific Trm precursors after LCMV infection, underlining a role in their retention within tissues. The early impact of Hobit and Blimp\u20101 favored Trm formation and prevented the development of circulating memory T cells. Thus, our findings highlight a role of Hobit and Blimp\u20101 at the branching point of circulating and resident memory lineages by suppressing tissue egress of Trm precursors early during infection.<\/jats:p>","DOI":"10.1002\/eji.202149665","type":"journal-article","created":{"date-parts":[[2022,4,7]],"date-time":"2022-04-07T14:44:31Z","timestamp":1649342671000},"page":"1095-1111","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Hobit and Blimp\u20101 regulate T<sub>RM<\/sub> abundance after LCMV infection by suppressing tissue exit pathways of T<sub>RM<\/sub>precursors"],"prefix":"10.1002","volume":"52","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4348-1679","authenticated-orcid":false,"given":"Loreto","family":"Parga\u2010Vidal","sequence":"first","affiliation":[{"name":"Department of Hematopoiesis Sanquin Research and Landsteiner Laboratory Amsterdam UMC University of Amsterdam  Amsterdam The 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