期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 52, 期 7, 页码 1095-1111出版社
WILEY
DOI: 10.1002/eji.202149665
关键词
Blimp-1; CD8(+) T-cell differentiation; Hobit; LCMV; tissue-resident memory CD8(+) T cells
类别
资金
- Vidi from ZonMw [917.13.338]
- Landsteiner Foundation of Blood Transfusion Research
- Alexander von Humboldt Foundation
- Veni from ZonMw [016.186.116]
Tissue-resident memory T cells (Trm) are retained in peripheral tissues after infection for enhanced protection against secondary encounter with the same pathogen. In this study, the transcription factors Hobit and Blimp-1 were found to play important roles in the formation and tissue retention of Trm.
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 Hobit and Blimp-1 were required for the upregulation of CD69 and suppression of CCR7 and S1PR1 on virus-specific Trm precursors after LCMV infection, underlining a role in their retention within tissues. The early impact of Hobit and Blimp-1 favored Trm formation and prevented the development of circulating memory T cells. Thus, our findings highlight a role of Hobit and Blimp-1 at the branching point of circulating and resident memory lineages by suppressing tissue egress of Trm precursors early during infection.
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