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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE271414 | 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 (scRNA-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 | GSE271415 | GEO

RIPK1 plays a crucial role in maintaining regulatory T cell homeostasis by inhibiting both RIPK3 and FADD-mediated cell death

Project description:Regulatory T (Treg) cells are a critical for maintaining immune balance in various physiological and pathological conditions. However, the mechanisms underlying Treg homeostasis remain incompletely understood. In this study, we demonstrated that RIPK1 is crucial for Treg cell survival and homeostasis. We generated mice with Treg cell-specific ablation of Ripk1 and found that these mice developed fatal systemic autoimmunity due to a dramatic reduction in the number of Treg cell caused by excessive cell death. Unlike conventional T cells, Treg cells with Ripk1 deficiency were only partially rescued from cell death by blocking the FADD pathway. However, simultaneous removal of both Fadd and Ripk3 completely restored the number of Ripk1-deficient Treg cells by blocking cell death. Our results demonstrated that RIPK1 plays a critical role in regulating Treg cell survival by controlling both necroptosis and apoptosis. These findings provide new insights into the mechanisms of Treg cell homeostasis and suggest potential therapeutic targets for autoimmune diseases.

2023-10-31 | GSE230483 | GEO

RIPK1 protects naïve and regulatory T cells from TNFR1-induced apoptosis

Project description:The T cell population size is stringently controlled before, during, and after immune responses, as improper cell death regulation can result in autoimmunity and immunodeficiency. RIPK1 is an important regulator of peripheral T cell survival and homeostasis. However, whether different peripheral T cell subsets show a differential requirement for RIPK1 and which programmed cell death pathway they engage in vivo remains unclear. In this study, we used mesenteric lymph node (mLN) cells of Ripk1 KO mice, Ripk1/Casp8 double KO mice and their respective wild types to investigate this.

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Foxp1 is critical for the maintenance of regulatory T-cell homeostasis and suppressive function

Project description:Regulatory T (Treg) cells play central roles in maintaining immune homeostasis and self-tolerance. However, the molecular mechanisms underlying Treg cell homeostasis and suppressive function are still not fully understood. Here, we report that the deletion of another P subfamily members of the forkhead box (Foxp) subfamily member Foxp1 in Treg cells led to increased numbers of activated Treg (aTreg) cells at the expense of quiescent Treg cells, and also resulted in impaired Treg suppressive function. Mice with Foxp1-deficient Treg cells developed spontaneous inflammatory disease with age; they also had more severe inflammatory disease in colitis and experimental autoimmune encephalomyelitis (EAE) models. Mechanistically, we found that Foxp1 bound to the conserved noncoding sequence 2 (CNS2) element of the Foxp3 locus and helped maintain Treg suppressive function by stabilizing the Foxp3 expression. Furthermore, we found that Foxp1 and Foxp3 coordinated the regulation of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression levels. Taken together, our study demonstrates that Foxp1 plays critical roles in both maintaining Treg cell quiescence during homeostasis and regulating Treg suppressive function.

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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

Lack of phosphatidylinositol 3-kinase VPS34 in regulatory T cells leads to a fatal lymphoproliferative disorder without affecting their development

Project description:Regulatory T (Treg) cells are essential for the maintenance of immunological tolerance, yet the molecular components required for their maintenance and effector functions remain incompletely defined. Inactivation of VPS34 in Treg cells led to an early, lethal phenotype, with massive effector T cell activation and inflammation, like mice lacking Treg cells completely. However, VPS34-deficient Treg cells developed normally, populated the peripheral lymphoid organs and effectively supressed conventional T cells in vitro. Our data suggest that VPS34 is required for the maturation of Treg cells or that mature Treg cells depend on VPS34 for survival. Functionally, we observed that lack of VPS34 activity impairs cargo processing upon transendocytosis, that defective autophagy contributes to, but is not sufficient to explain this lethal phenotype, and that loss of VPS34 activity induces a state of heightened metabolic activity that may interfere with metabolic networks required for maintenance or suppressive functions of Treg cells.

2024-01-29 | PXD048981 | Pride

Transcription profiling of mouse Cbfb-deficient regulatory T cells

Project description:Gene expression profiles of Cbfb-deficient and control Treg cells were compared. Abstract: Naturally arising regulatory T (Treg) cells express the transcription factor FoxP3, which critically controls the development and function of Treg cells. FoxP3 interacts with another transcription factor Runx1 (also known as AML1). Here we showed that Treg cell-specific deficiency of Cbfβ, a cofactor for all Runx proteins, or that of Runx1, but not Runx3, induced lymphoproliferation, autoimmune disease, and hyper-production of IgE. Cbfb-deleted Treg cells exhibited impaired suppressive function in vitro and in vivo, with altered gene expression profiles including attenuated expression of FoxP3 and high expression of interleukin-4. The Runx complex bound to more than 3000 gene loci in Treg cells, including the Foxp3 regulatory regions and the Il4 silencer. In addition, knockdown of RUNX1 showed that RUNX1 is required for the optimal regulation of FoxP3 expression in human T cells. Taken together, our results indicate that the Runx1-Cbfβ heterodimer is indispensable for in vivo Treg cell function, in particular, suppressive activity and optimal expression of FoxP3. Experiment Overall Design: CD4+CD25hi cells, most of which were Foxp3+ Treg cells, were isolated from Cbfb-flox/flox: Foxp3-ires-Cre (n = 3) and control Cbfb-flox/wt: Foxp3-ires-Cre (n = 3) mice. Total RNA was extracted from those purified Cbfb-deficient or control Treg cells.

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T cell-specific RIPK1 ablation results in villus atrophy of the duodenum in mice

Project description:RIPK1 is required in T cells with a history of CD4-expression to maintain intestinal homeostasis. We show that the pathology in the upper intestine is a result of conventional T cell apoptosis in absence of the RIPK1.

2025-03-05 | GSE263990 | GEO

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