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The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses [RNA-Seq]

ABSTRACT: These are spleen and kidney T cells directly analyzed from the indicated mice by RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE192953 | GEO | 2022/08/09

REPOSITORIES: GEO

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The ZFP36 family of RNA binding proteins regulates homeostatic and autoreactive T cell responses.

Project description:RNA binding proteins are important regulators of T cell activation, proliferation, and cytokine production. The zinc finger protein 36 (ZFP36) family genes (Zfp36, Zfp36l1, and Zfp36l2) encode RNA binding proteins that promote the degradation of transcripts containing AU-rich elements. Numerous studies have demonstrated both individual and shared functions of the ZFP36 family in immune cells, but their collective function in T cells remains unclear. Here, we found a redundant and critical role for the ZFP36 proteins in regulating T cell quiescence. T cell-specific deletion of all three ZFP36 family members in mice resulted in early lethality, immune cell activation, and multiorgan pathology characterized by inflammation of the eyes, central nervous system, kidneys, and liver. Mice with T cell-specific deletion of any two Zfp36 genes were protected from this spontaneous syndrome. Triply deficient T cells overproduced proinflammatory cytokines, including IFN-γ, TNF, and GM-CSF, due to increased mRNA stability of these transcripts. Unexpectedly, T cell-specific deletion of both Zfp36l1 and Zfp36l2 rendered mice resistant to experimental autoimmune encephalomyelitits due to failed priming of antigen-specific CD4+ T cells. ZFP36L1 and ZFP36L2 double-deficient CD4+ T cells had poor proliferation during in vitro T helper cell polarization. Thus, the ZFP36 family redundantly regulates T cell quiescence at homeostasis, but ZFP36L1 and ZFP36L2 are specifically required for antigen-specific T cell clonal expansion.

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The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-08 | GSE192956 | GEO

The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses [mRNA-decaySeq]

Project description:These are CD44hi CD4 T splenic T cells from the indicated mice activated in vitro with anti-CD3/anti-CD28 for 24 hours. Following activation, cells were treated with Actinomycin D for the indicated time course.

2022-08-09 | GSE192954 | GEO

The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses

Project description:The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses

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The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses [RNA-Seq]

Project description:The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses [RNA-Seq]

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The ZFP36 family of RNA-binding proteins regulates homeostatic and autoreactive T cell responses [mRNA-decaySeq]

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ZFP36-family RNA-binding proteins in regulatory T cells reinforce immune homeostasis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-08 | GSE244621 | GEO

ZFP36 RNA-binding proteins restrain T cell activation and anti-viral immunity.

Project description:Dynamic post-transcriptional control of RNA expression by RNA-binding proteins (RBPs) is critical during immune response. ZFP36 RBPs are prominent inflammatory regulators linked to autoimmunity and cancer, but functions in adaptive immunity are less clear. We used HITS-CLIP to define ZFP36 targets in mouse T cells, revealing unanticipated actions in regulating T-cell activation, proliferation, and effector functions. Transcriptome and ribosome profiling showed that ZFP36 represses mRNA target abundance and translation, notably through novel AU-rich sites in coding sequence. Functional studies revealed that ZFP36 regulates early T-cell activation kinetics cell autonomously, by attenuating activation marker expression, limiting T cell expansion, and promoting apoptosis. Strikingly, loss of ZFP36 in vivo accelerated T cell responses to acute viral infection and enhanced anti-viral immunity. These findings uncover a critical role for ZFP36 RBPs in restraining T cell expansion and effector functions, and suggest ZFP36 inhibition as a strategy to enhance immune-based therapies.

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ZFP36-family RNA-binding proteins in regulatory T cells reinforce immune homeostasis [bulk RNA-seq]

Project description:RNA binding proteins (RBP) of the ZFP36 family limit the differentiation and effector functions of CD4 and CD8 T cells, but little is known of their expression or function in regulatory T cells (Treg). By Treg-restricted deletion of Zfp36 family members we identify the essential role of Zfp36l1 and Zfp36l2 in Treg to maintain immune homeostasis. Mice with Tregs deficient in these RBP display an inflammatory phenotype with an expansion in the numbers of type-2 conventional dendritic cells, T effector cells, T follicular helper and germinal center B cells and elevated serum cytokines and immunoglobulins. In the absence of Zfp36l1 and Zfp36l2, the pool of cycling CTLA-4 in naïve Treg was reduced, Tregs were less sensitive to IL-2 and IL-7 but were more sensitive to IFNγ. In mice lacking both RBP in Treg, the deletion of a single allele of Ifng is sufficient to ameliorate the pathology. Thus, ZFP36L1 and ZFP36L2 regulate multiple pathways that enable Tregs to enforce immune homeostasis.

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