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Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE271416 | GEO | 2025/07/01

REPOSITORIES: GEO

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Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (RNA-Seq)

Project description:Ripk1 plays an important role as a regulator of programmed cell death processes such as apoptosis and necroptosis, and is involved in the initiation of pro-inflammatory NF-kB signaling. Immune tolerance depends on the proper function and homeostasis of regulatory T cells. Here, we show that Treg-specific ablation of Ripk1 in mice leads to a reduction of Treg cells and spontaneous systemic autoimmunity. Using chimeric mice that allowed us to study Treg cells in the absence of inflammatory conditions, we observed a disadvantage of Ripk1-deficient compared to Ripk1-proficient Treg cells. Importantly, we did not observe impaired viability of the Ripk1-deficient Treg cells. Furthermore, single-cell RNA sequencing revealed that Ripk1 is required for the maintenance of the Treg cell transcriptional signature, which is essential for the suppressive function of Treg cells. Together, these findings highlight the fundamental role of Ripk1 in maintaining immune homeostasis by preserving the suppressive phenotype of Treg cells

2025-07-01 | GSE271414 | GEO

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (scRNA-Seq)

2025-07-01 | GSE271415 | GEO

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells

Project description:Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells

| PRJNA1131354 | ENA

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (scRNA-Seq)

Project description:Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (scRNA-Seq)

| PRJNA1131361 | ENA

Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (RNA-Seq)

Project description:Ripk1 is critical for preserving effector regulatory T cells and the suppressive transcriptional program in regulatory T cells (RNA-Seq)

| PRJNA1131362 | ENA

JunB modulates an IRF4-dependent transcriptional program to regulate homeostasis and suppressive functions of effector regulatory T cells

Project description:To understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq and ChIP-seq analyses of JunB-deficient and control Treg cells (CD4+ CD25hi). This SuperSeries is composed of the SubSeries listed below.

2018-11-19 | GSE121295 | GEO

JunB regulates homeostasis and suppressive functions of effector regulatory T cells.

Project description:Foxp3-expressing CD4+ regulatory T (Treg) cells need to differentiate into effector Treg (eTreg) cells to maintain immune homeostasis. T-cell receptor (TCR)-dependent induction of the transcription factor IRF4 is essential for eTreg differentiation, but how IRF4 activity is regulated in Treg cells is still unclear. Here we show that the AP-1 transcription factor, JunB, is expressed in eTreg cells and promotes an IRF4-dependent transcription program. Mice lacking JunB in Treg cells develop multi-organ autoimmunity, concomitant with aberrant activation of T helper cells. JunB promotes expression of Treg effector molecules, such as ICOS and CTLA4, in BATF-dependent and BATF-independent manners, and is also required for homeostasis and suppressive functions of eTreg. Mechanistically, JunB facilitates the accumulation of IRF4 at a subset of IRF4 target sites, including those located near Icos and Ctla4. Thus, JunB is a critical regulator of IRF4-dependent Treg effector programs, highlighting important functions for AP-1 in Treg-mediated immune homeostasis.

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Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells.

Project description:Regulatory T (Treg) cells are critical in regulating the immune response. In vitro induced Treg (iTreg) cells have significant potential in clinical medicine. However, applying iTreg cells as therapeutics is complicated by the poor stability of human iTreg cells and their variable suppressive activity. Therefore, it is important to understand the molecular mechanisms of human iTreg cell specification. We identified hypermethylated in cancer 1 (HIC1) as a transcription factor upregulated early during the differentiation of human iTreg cells. Although FOXP3 expression was unaffected, HIC1 deficiency led to a considerable loss of suppression by iTreg cells with a concomitant increase in the expression of effector T cell associated genes. SNPs linked to several immune-mediated disorders were enriched around HIC1 binding sites, and in vitro binding assays indicated that these SNPs may alter the binding of HIC1. Our results suggest that HIC1 is an important contributor to iTreg cell development and function.

| S-EPMC5842026 | biostudies-literature

The lineage stability and suppressive program of regulatory T cells require protein O-GlcNAcylation.

Project description:Regulatory T (Treg) cells control self-tolerance, inflammatory responses and tissue homeostasis. In mature Treg cells, continued expression of FOXP3 maintains lineage identity, while T cell receptor (TCR) signaling and interleukin-2 (IL-2)/STAT5 activation support the suppressive effector function of Treg cells, but how these regulators synergize to control Treg cell homeostasis and function remains unclear. Here we show that TCR-activated posttranslational modification by O-linked N-Acetylglucosamine (O-GlcNAc) stabilizes FOXP3 and activates STAT5, thus integrating these critical signaling pathways. O-GlcNAc-deficient Treg cells develop normally but display modestly reduced FOXP3 expression, strongly impaired lineage stability and effector function, and ultimately fatal autoimmunity in mice. Moreover, deficiency in protein O-GlcNAcylation attenuates IL-2/STAT5 signaling, while overexpression of a constitutively active form of STAT5 partially ameliorates Treg cell dysfunction and systemic inflammation in O-GlcNAc deficient mice. Collectively, our data demonstrate that protein O-GlcNAcylation is essential for lineage stability and effector function in Treg cells.

| S-EPMC6341091 | biostudies-literature

Human regulatory T cell suppressive function is independent of apoptosis induction in activated effector T cells.

Project description:CD4(+)CD25(+)FOXP3(+) Regulatory T cells (Treg) play a central role in the immune balance to prevent autoimmune disease. One outstanding question is how Tregs suppress effector immune responses in human. Experiments in mice demonstrated that Treg restrict effector T cell (Teff) responses by deprivation of the growth factor IL-2 through Treg consumption, resulting in apoptosis of Teff.In this study we investigated the relevance of Teff apoptosis induction to human Treg function. To this end, we studied naturally occurring Treg (nTreg) from peripheral blood of healthy donors, and, to investigate Treg function in inflammation in vivo, Treg from synovial fluid of Juvenile Idiopathic Arthritis (JIA) patients (SF-Treg). Both nTreg and SF-Treg suppress Teff proliferation and cytokine production efficiently as predicted. However, in contrast with murine Treg, neither nTreg nor SF-Treg induce apoptosis in Teff. Furthermore, exogenously supplied IL-2 and IL-7 reverse suppression, but do not influence apoptosis of Teff.Our functional data here support that Treg are excellent clinical targets to counteract autoimmune diseases. For optimal functional outcome in human clinical trials, future work should focus on the ability of Treg to suppress proliferation and cytokine production of Teff, rather than induction of Teff apoptosis.

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