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Homeostasis and transitional activation of regulatory T cells require c-Myc

ABSTRACT: Homeostasis and transitional activation of regulatory T cells require c-Myc

PROVIDER: PRJNA593657 | ENA |

REPOSITORIES: ENA

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Homeostasis and transitional activation of regulatory T cells require c-Myc

Project description:Regulatory T (Treg) cell activation and expansion during neonatal life and in response to inflammation are critical for immunosuppression, yet the mechanisms governing these events are incompletely understood. We report that the oncogene and transcriptional regulator c-Myc (Myc) controls immune homeostasis through regulation of Treg cell accumulation and functional activation. Myc activity is enriched in Treg cells generated during neonatal life and responding to inflammation. Myc-deficient Treg cells show cell-intrinsic defects in overall accumulation and ability to transition to an activated state during early life or acute inflammation. Consequently, loss of Myc in Treg cells results in a rapid, early-onset autoimmune disorder accompanied by uncontrolled effector CD4+ and CD8+ T cell responses. We also provide evidence that Myc regulates mitochondrial oxidative metabolism but is dispensable for fatty acid oxidation (FAO). Indeed, Treg cell-specific deletion of Cox10, which is required for oxidative phosphorylation, but not Cpt1a, the rate-limiting enzyme for FAO, results in impaired Treg cell function and maturation. Thus, Myc coordinates Treg cell accumulation, transitional activation and metabolic programming to orchestrate immune homeostasis. We used microarrays to compare the global transcription profiles of WT and Myc-null Treg cells.

2020-01-10 | GSE141499 | GEO

Homeostasis and transitional activation of regulatory T cells require c-Myc.

Project description:Regulatory T cell (Treg) activation and expansion occur during neonatal life and inflammation to establish immunosuppression, yet the mechanisms governing these events are incompletely understood. We report that the transcriptional regulator c-Myc (Myc) controls immune homeostasis through regulation of Treg accumulation and functional activation. Myc activity is enriched in Tregs generated during neonatal life and responding to inflammation. Myc-deficient Tregs show defects in accumulation and ability to transition to an activated state. Consequently, loss of Myc in Tregs results in an early-onset autoimmune disorder accompanied by uncontrolled effector CD4+ and CD8+ T cell responses. Mechanistically, Myc regulates mitochondrial oxidative metabolism but is dispensable for fatty acid oxidation (FAO). Indeed, Treg-specific deletion of Cox10, which promotes oxidative phosphorylation, but not Cpt1a, the rate-limiting enzyme for FAO, results in impaired Treg function and maturation. Thus, Myc coordinates Treg accumulation, transitional activation, and metabolic programming to orchestrate immune homeostasis.

| S-EPMC6938709 | biostudies-literature

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis

Project description:Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis

| PRJNA607766 | ENA

Immune homeostasis and regulation of the Interferon pathway require myeloid-derived Regnase-3

Project description:Immune homeostasis and regulation of the Interferon pathway require myeloid-derived Regnase-3

| PRJNA530962 | ENA

Congenital T cell activation blocks transitional to follicular B cell maturation in humans

Project description:In patients with CTLA4 deficiency, CD40L-expressing T cells inhibit transitional to follicular B cell maturation in the T cell zone of lymph nodes through the induction of mTORC1 signaling in transitional B cells. We apply scRNA-seq to identify upregulation of PI3K, mTORC1, and oxidative phosphorylation pathways in patients with CTLA4 deficiency, and to characterize resolution of follicular block after treatment with abatacept.

2021-11-10 | GSE188449 | GEO

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (ChIP-Seq).

Project description:Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (ChIP-Seq).

| PRJNA607770 | ENA

Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (RNA-Seq).

Project description:Pancreatic cancer cells require the transcription factor MYRF (Myelin Regulatory Factor) to maintain ER homeostasis (RNA-Seq).

| PRJNA607769 | ENA

Proteome profiling upon Myc activation

Project description:The effect of Myc activation on the proteome was investigated in U2OS cells and proteome changes were combined with Ribo-seq, RNA-seq and GRO-seq analyses.

2015-11-09 | PXD002073 | Pride

Regulation of MYC by CARD14 in Human Epithelium is a Determinant of Epidermal Homeostasis and Disease II

Project description:Caspase recruitment domain family member 14 (CARD14) and its variants are associated with both atopic dermatitis (AD) and psoriasis, but their mechanistic impact on skin barrier homeostasis is largely unknown. CARD14 is known to signal via NFκB, however, CARD14-NFκB signaling does not fully explain the heterogeneity of CARD14-driven disease. Herein, we describe a direct interaction between CARD14 and MYC and show that CARD14 signals through MYC in keratinocytes to coordinate skin barrier homeostasis. CARD14 directly binds MYC and influences barrier formation in a MYC-dependent fashion, and this mechanism is undermined by disease-associated CARD14 variants. These studies establish a paradigm that CARD14 activation regulates skin barrier function by two distinct mechanisms including activating NFκB to bolster the antimicrobial (chemical) barrier and stimulating MYC to bolster the physical barrier. Finally, we show that CARD14-dependent MYC signaling occurs in other epithelia expanding the impact of our findings beyond the skin.

2024-07-13 | GSE263428 | GEO

Regulation of MYC by CARD14 in Human Epithelium is a Determinant of Epidermal Homeostasis and Disease I

2024-07-13 | GSE263420 | GEO

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