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Innate versus adaptive lymphoid cell fate choice is controlled by the E-Id protein axis

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

ORGANISM(S): Mus musculus

PROVIDER: GSE95339 | GEO | 2017/06/01

SECONDARY ACCESSION(S): PRJNA376684

REPOSITORIES: GEO

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Innate versus adaptive lymphoid cell fate choice is controlled by the E-Id protein axis [ATAC-Seq]

Project description:The lymphoid branch of the immune defense is composed of innate and adaptive immune cells. Using multiple genetic strategies we demonstrate that in the thymus E2A and HEB act in synergy to establish T cell identity and to suppress the aberrant development of innate lymphoid cells that include ILC2 and LTi-like cells. We found that E2A and HEB induce T cell fate by activating the expression of an ensemble of genes encoding for proteins associated with Notch- and pre-TCR signaling and to promote TCRβ antigen receptor assembly. We show that E2A and HEB act in early T progenitors (ETPs) to establish and maintain a T-lineage specific enhancer repertoire, including regulatory elements associated with the Notch1/3 and Rag1/2 gene loci. Based on these and previous observations we propose that the E-Id protein axis specifies innate versus adaptive lymphoid cell fate.

2017-06-01 | GSE95338 | GEO

Innate versus adaptive lymphoid cell fate choice is controlled by the E-Id protein axis [RNA-Seq]

2017-06-01 | GSE95337 | GEO

Innate versus adaptive lymphoid cell fate choice is controlled by the E-Id protein axis

Project description:Innate versus adaptive lymphoid cell fate choice is controlled by the E-Id protein axis

| PRJNA376684 | ENA

The E-Id Protein Axis Specifies Adaptive Lymphoid Cell Identity and Suppresses Thymic Innate Lymphoid Cell Development.

Project description: Not available

| S-EPMC5512722 | biostudies-literature

Regulation of lymphoid versus myeloid fate choice by Mef2c

Project description:Despite recent advances in the identification of lymphoid-restricted progenitors, the transcription factors essential for their generation remain to be identified. Here we describe an unexpected role for the myeloid oncogene Mef2c in multipotent progenitors (MPPs), where it is required for pan-lymphoid differentiation. Mef2c deficiency was associated with profound defects in B, T, NK cell and common lymphoid progenitor production and an enhanced myeloid output. Mef2c deficiency in MPPs leads to downregulation of several key lymphoid regulators and the upregulation of the myeloid factor C/EBPa. Our studies also show that Mef2c is a critical transcriptional target of PU.1 during lymphopoiesis. Thus, Mef2c is a crucial component of the transcriptional network that regulates lymphoid specification and cell fate choice in MPPs.

2008-11-21 | GSE13686 | GEO

Distinct Gene Regulatory Pathways for Human Innate versus Adaptive Lymphoid Cells.

Project description: Not available

| S-EPMC4874868 | biostudies-literature

Distinct Gene Regulatory Pathways for Human Innate Versus Adaptive Lymphoid Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-13 | E-GEOD-78897 | biostudies-arrayexpress

Distinct and shared gene expression for human innate versus adaptive helper lymphoid cells.

Project description: Not available

| S-EPMC7496918 | biostudies-literature

Distinct Gene Regulatory Pathways for Human Innate Versus Adaptive Lymphoid Cells

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

2016-05-13 | GSE78897 | GEO

Distinct Gene Regulatory Pathways for Human Innate Versus Adaptive Lymphoid Cells [gene expression]

Project description:Innate lymphoid cells (ILCs) serve as sentinels in mucosal tissues, sensing release of soluble inflammatory mediators, rapidly communicating danger via cytokine secretion, and functioning as guardians of tissue homeostasis. Although ILCs have been studied extensively in model organisms, little is known about these âfirst respondersâ in humans, especially their lineage and functional kinships to cytokine-secreting T helper cell (Th) counterparts. Here, we report gene regulatory circuitries for four human ILCâTh counterparts derived from mucosal environments, revealing that each ILC subset diverges as a distinct lineage from Th and circulating natural killer cells, but shares circuitry devoted to functional polarization with their Th counterparts. Super-enhancers demarcate cohorts of cell identity genes in each lineage, uncovering new modes of regulation for signature cytokines, novel molecules that likely impart important functions to ILCs, and potential mechanisms for autoimmune disease SNP associations within ILCâTh subsets. RNA was isolated from two to five replicates of ILC1, ILC3, Th1, Th2 and NK cells. Gene expression levels were determined using Affymetrix Human Gene 1.0 ST arrays.

2016-05-13 | E-GEOD-78896 | biostudies-arrayexpress

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