Dataset Information

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 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.

SUBMITTER: Parga-Vidal L

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

REPOSITORIES: biostudies-literature

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Publications

Hobit and Blimp-1 regulate T<sub>RM</sub> abundance after LCMV infection by suppressing tissue exit pathways of T<sub>RM</sub> precursors.

Parga-Vidal Loreto L Taggenbrock Renske L R E RLRE Beumer-Chuwonpad Ammarina A Aglmous Hajar H Kragten Natasja A M NAM Behr Felix M FM Bovens Astrid A AA van Lier Rene A W RAW Stark Regina R van Gisbergen Klaas P J M KPJM

European journal of immunology 20220415 7

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 impa ...[more]

PMID: 35389518

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Project description:The tailbud is a population of stem cells in the posterior embryonic tail. During zebrafish development, these stem cells give rise to the main structures of the embryo's posterior body, including the tail somites. Progenitor cells reside in the tailbud for variable amounts of time before they exit and begin to differentiate. There must be a careful balance between cells that leave the tailbud and cells that are held back in order to give rise to later somites. However, this meticulous process is not well understood. A gene that has shed some light on this area is the t-box transcription factor spadetail (spt). When spt is mutated, embryos develop an enlarged tailbud and are only able to form roughly half of their somites. This phenotype is due to the fact that some of the somitic precursors are not able to leave the tailbud or differentiate. Another factor involved in tail morphogenesis is the Bone Morphogenetic Protein (BMP) pathway. BMPs are important for many processes during early development, including cell migration. Chordino (chd) is a secreted protein that inhibits BMP signaling. BMPs are upregulated in chd mutants, however, these mutants are able to form organized somites. In embryos where chd and spt are mutated, somites are completely absent. These double mutants also develop a large tailbud due to the accumulation of progenitor cells that are never able to leave or differentiate. To study the dynamics of cells in the tailbud and their role in somite formation, we have analyzed the genetic factors and pathway interactions involved, conducted transplant experiments to look at behavior of mutant cells in different genetic backgrounds, and used time lapse microscopy to characterize cell movements and behavior in wild type and mutant tailbuds. These data suggest that spt expression and BMP inhibition are both required for somitic precursors to exit the tailbud. They also elucidate that chd;spt tailbud mesodermal progenitor cells (MPC) behave autonomously and their dynamics within the tailbud are drastically different than WT MPCs.

Dataset Information

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

Publications

Hobit and Blimp-1 regulate T<sub>RM</sub> abundance after LCMV infection by suppressing tissue exit pathways of T<sub>RM</sub> precursors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

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

Publications

Hobit and Blimp-1 regulate T<sub>RM</sub> abundance after LCMV infection by suppressing tissue exit pathways of T<sub>RM</sub> precursors.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

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