Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA352830 | ENA |
REPOSITORIES: ENA
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Project description:Studies over the past decade characterized murine regulatory T cells (Tregs) with the capacity to promote tissue regeneration. In humans, such a population of tissue-repair Treg cells has not been discovered yet. Using single-cell chromatin accessibility profiles of murine and human tissue Treg cells, we defined a species-conserved and microbiota-independent repair Treg signature, with a prevailing footprint of the transcription factor BATF. Combining this signature with gene expression profiling and TCR fate mapping, we identified a population of tissue-like Treg cells in peripheral blood, characterized by the expression of BATF, CCR8 and HLA-DR. Human BATF+CCR8+ Treg cells from normal skin and adipose tissue shared features with tumor-resident Treg and tissue T-follicular helper (Tfh) cells. Inducing a Tfh-like differentiation program in naive Treg cells partially recapitulated human tissue Treg characteristics, including enhanced wound healing potential
| EGAS00001004900 | EGA
Project description:Purpose: Identification of the differentially expressed genes and metabolic pathways in resting and activated WT and BATF-deficient Treg cells Methods: RNA was purified from resting of stimulated (aCD3-CD38/IL-2 for 48 h)Treg cells isolated from WT or Foxp3CreBatffl/fl mice Results: Loss of BATF promotes triacylglycerol biosynthesis in Treg cells. Conclusions: BATF is crucial to coordinate the suppressive function and triacylglycerol metabolism of Treg cells.
2021-03-02 | GSE149197 | GEO
Project description:T cells that encounter self-antigens after exiting the thymus avert autoimmunity through peripheral tolerance. Pathways for this include an unresponsive state known as anergy, clonal deletion, and T regulatory (Treg) cell induction. The transcription factor cues and kinetics that guide distinct peripheral tolerance outcomes remain unclear. Here, we found that anergic T cells are epigenetically primed for regulation by the non-classical AP-1 family member BATF. Tolerized BATF-deficient CD4+ T cells were resistant to anergy induction and instead underwent clonal deletion due to pro-apoptotic BIM (Bcl2l11) upregulation. During prolonged antigen exposure, BIM de-repression resulted in fewer PD-1+ conventional T cells as well as loss of peripherally-induced FOXP3+ Treg cells. Simultaneous Batf and Bcl2l11 knockdown meanwhile restored anergic T cell survival and Treg cell maintenance. The data identify the AP-1 nuclear factor BATF as a dominant driver of sustained T cell anergy and illustrate a mechanism for divergent peripheral tolerance fates.
2023-10-17 | GSE244276 | GEO
Project description:Th17 cells secrete IL-17A, IL-17F, IL-21, and IL-22 cytokines that are critical in mediating inflammation and protecting the host from microorganisms infection. The basic leucine zipper transcription factor ATF-like (Batf) contributes to the transcriptional programming of multiple effector T cells, and is required for Th17 cell development. Here, we have interrogated mechanisms by which Batf promotes and stabilizes Th17 cell phenotype. We have shown that in vitro differentiated Th17 cells have increased expression of Th1 and Treg signature genes in the absence of Batf. In addition, Citrobacter rodentium infected Batf-deficient (Batf KO) mice fail to clear the infection, and that is correlated with diminished IL-17A and IL-22 cytokine production and increased Foxp3 and Ifng expression compared to WT mice. We find that Batf sustains Th17 phenotype in long-term culture conditions by suppressing Th1- and Treg-specific gene expression. Mechanistically, we reveal that Batf negatively regulates IL-2-STAT5 signaling and modulates STAT5 binding at the Ifng and Foxp3 gene loci thus suppressing Th1-Treg phenotype in Th17 cell development. Inhibition of STAT5 DNA binding activity in Batf KO Th17 cells was able to repress Ifng and Foxp3 expression compared to control-treated cells. Moreover, STAT5 cooperates with transcription factors Ets1 and Runx1 to mediate epigenetic modification and regulate gene expression. Thus, our study has revealed an essential function of Batf in modulating the IL-2-STAT5 signaling to promote and stabilize Th17 cell development.
2023-04-26 | GSE167417 | GEO
Project description:Expression data of Naïve Treg and Tumor associated Treg cells
| PRJNA109769 | ENA
Project description:Expression data on Treg cells isolated from wildtype mice and miR-125a deficient mice
| PRJNA277459 | ENA
Project description:We collected whole genome testis expression data from hybrid zone mice. We integrated GWAS mapping of testis expression traits and low testis weight to gain insight into the genetic basis of hybrid male sterility.
2014-12-04 | GSE61417 | GEO
Project description:Regulatory T (Treg) cells suppress effective antitumor immunity in tumor-bearing hosts, thereby becoming promising targets in cancer immunotherapy. Here, we show that Treg cells in the tumor microenvironment (TME) of human lung cancers harbor a completely different open chromatin profile compared to effector T cells and peripheral Treg cells. The integrative sequencing analyses revealed that BATF, IRF4, NF-κb, and NR4A were important transcription factors for Treg cell differentiation in the TME. Particularly, BATF was identified as a key regulator, which leveraged Treg cell differentiation through epigenetically controlling activation-associated gene expression, resulting in the robustness of Treg cells in the TME. BATF deficiency in Treg cells remarkably inhibited tumor growth and high BATF expression was associated with poor prognosis in lung cancer, kidney cancer, and melanoma. Our results propose the specific chromatin remodeling and differentiation program of Treg cells in the TME, which can be applied in the development of Treg cell-targeted therapies.
2022-08-22 | GSE211153 | GEO
Project description:Regulatory T (Treg) cells suppress effective antitumor immunity in tumor-bearing hosts, thereby becoming promising targets in cancer immunotherapy. Here, we show that Treg cells in the tumor microenvironment (TME) of human lung cancers harbor a completely different open chromatin profile compared to effector T cells and peripheral Treg cells. The integrative sequencing analyses revealed that BATF, IRF4, NF-κb, and NR4A were important transcription factors for Treg cell differentiation in the TME. Particularly, BATF was identified as a key regulator, which leveraged Treg cell differentiation through epigenetically controlling activation-associated gene expression, resulting in the robustness of Treg cells in the TME. BATF deficiency in Treg cells remarkably inhibited tumor growth and high BATF expression was associated with poor prognosis in lung cancer, kidney cancer, and melanoma. Our results propose the specific chromatin remodeling and differentiation program of Treg cells in the TME, which can be applied in the development of Treg cell-targeted therapies.
2022-08-22 | GSE211087 | GEO