Hobit and Blimp-1 regulate T_RM abundance after LCMV infection by suppressing tissue exit pathways of T_RM precursors.

ABSTRACT: Tissue-resident memory T cells (Trm) are retained in peripheral tissues after infection for enhanced protection against secondary encounter with the same pathogen. We have previously shown that the transcription factor Hobit and its homolog Blimp-1 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-1 in regulating several aspects of effector T-cell 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-1 in Trm, allowing us to specifically investigate the role of both transcription factors in Trm differentiation. We found that H

SUBMITTER: Parga-Vidal L 

PROVIDER: S-EPMC9545210 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature