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Zfp335 establishes eTreg lineage and neonatal immune tolerance by targeting Hadha-mediated fatty acid oxidation

ABSTRACT: We utilized single-cell RNA sequencing (scRNA-seq) to carry out comparative transcriptome analysis in Tregs from the spleens of WT and KO (Zfp335fl/flFoxp3-Cre).

ORGANISM(S): Mus musculus

PROVIDER: GSE189058 | GEO | 2023/10/10

REPOSITORIES: GEO

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Zfp335 establishes neonatal immune tolerance through safeguarding effector Treg lineage commitment and maintenance

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Zfp335 establishes eTreg lineage and neonatal immune tolerance by targeting Hadha-mediated fatty acid oxidation

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Zfp335 establishes neonatal immune tolerance through safeguarding effector Treg lineage commitment and maintenance [ChIP-seq]

Project description:Regulatory T (Treg) cells are crucial for maintaining peripheral immune tolerance and preventing destructive autoreactive responses, but how heterogeneous Treg populations establish tolerant status remains unclear. Here, we found that Zinc finger protein 335 (Zfp335) is indispensable for the differentiation and maintenance of effector Treg (eTreg) population and immunological self-tolerance in neonates. Mice with Zfp335 deletion in Treg cells exhibit early-onset autoimmune disease with severe inflammation in multiple organs and unrestricted activation and expansion of conventional T cells. Zfp335-deficient Treg cells display dysfunctional and pathogenic features together with multiple defects in proliferation, survival and suppressive function. Importantly, our single-cell RNA sequencing (scRNA-seq) analyses reveal distinct Treg populations and that Zfp335 deficiency causes an almost complete loss of eTreg population along with significant accumulation of dysfunctional Treg populations. Mechanistically, Zfp335 controls both fate decision and homeostasis of eTreg cells by directly targeting genes associated with homeostasis and oxidation-fueled oxidative phosphorylation (OXPHOS) and PI3K-Akt-mTOR metabolic pathways. Our data establish the concept that Zfp335 serves as a checkpoint and safeguard for eTreg lineage commitment and maintenance.

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Gene expression profiling of CD4+CD25+Foxp3+ regulatory T cells and CD4+CD25-Foxp3- T cells in the course of Plasmodium yoelii infection of BALB/c mice

Project description:The objective of the present study was to characterize the phenotype of CD4+CD25+Foxp3+ regulatory T cells (Tregs) in the course of parasitic Plasmodium yoelii (P .yoelii) infection of BALB/c mice. Therefore we performed microarray expression analysis of CD4+CD25+Foxp3+ Tregs isolated by FACS from spleens of non-infected mice and from spleens of mice infected with P. yoelii 3 days and 5 days post infection. By comparing the gene expression profiles, we were able to identify molecules which were differentially expressed by Tregs during parasitic infection and thereby might be involved in their immune-suppressive function. Moreover, we included CD4+CD25-Foxp3- T cells from spleens of non-infected and P. yoelii-infected mice in our analysis. It was proposed that immune-suppressive CD4+CD25-Foxp3- T cells might be induced during Plasmodium infection of mice. Thus, detailed gene expression data of these cells in comparison to CD4+CD25+Foxp3+ Tregs would contribute a better understanding in the phenotype. FACS sorted CD4+CD25+Foxp3+ Tregs and CD4+CD25-Foxp3- T cells from pooled spleens of non-infected Foxp3/ eGFP mice (served as reference) and from pooled spleens of P. yoelii infected Foxp3/ eGFP mice 3 days and 5 days post infection were analyzed as single probes.

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