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Unregulated APC activation by T cells breaks self-tolerance

ABSTRACT: Unregulated APC activation by T cells breaks self-tolerance

PROVIDER: PRJNA498714 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8115050_1.fastq.gz	Fastqsanger.gz
	SRR8115050_2.fastq.gz	Fastqsanger.gz
	SRR8115045_1.fastq.gz	Fastqsanger.gz
	SRR8115045_2.fastq.gz	Fastqsanger.gz
	SRR8115046_1.fastq.gz	Fastqsanger.gz

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Unregulated APC activation by T cells breaks self-tolerance

Project description:The absence of nTregs results in slight increase of B7 on dendritic cells (DC). Such slightly elevated B7 induce proliferation of T cells with intrinic high self-affinity: bidirectional T/DC interaction ensues, leading to progressive DC activation and reciprocal strong T cell activation.

2019-01-23 | GSE121882 | GEO

Loss of self-tolerance leads to altered gene expression and IMD pathway activation in Drosophila melanogaster

Project description:Immune self-tolerance is the ability of a host’s immune system to recognize and avoid triggering immune responses against self-tissue. This allows the host to avoid self-directed immune damage, while still responding appropriately to pathogen infection. A breakdown of self-tolerance can lead to an autoimmune state in which immune cells target healthy self-tissue, leading to inflammation and tissue damage. In order to better understand the basic biology of autoimmunity and the role of the innate immune system in maintaining self-tolerance, we have recently characterized the Drosophila melanogaster tuSz autoimmune mutant. This mutant strain can serve as a model of innate immune mediated self-tolerance, and here we identify transcripts that are deregulated in flies experiencing a loss of self-tolerance. We found that these changes include the ectopic activation of pro-inflammatory signaling through the Relish/NFκB transcription factor, alterations in transcripts encoding proteins predicted to mediate organismal metabolism, and a downregulation of transcripts linked to developmental processes. This study can provide insight into the transcriptional and physiological changes underlying self-tolerance and autoimmunity.

2024-11-12 | GSE189383 | GEO

Thymic mimetic cells function beyond self-tolerance

Project description:Thymic mimetic cells function beyond self-tolerance

| PRJNA988538 | ENA

Thymic mimetic cells function beyond self-tolerance [Insm1]

Project description:Thymic mimetic cells function beyond self-tolerance [Insm1]

| PRJNA988544 | ENA

Thymic mimetic cells function beyond self-tolerance [mimetics]

Project description:Thymic mimetic cells function beyond self-tolerance [mimetics]

| PRJNA988542 | ENA

Thymic mimetic cells function beyond self-tolerance [Spib]

Project description:Thymic mimetic cells function beyond self-tolerance [Spib]

| PRJNA988546 | ENA

Unregulated antigen-presenting cell activation by T cells breaks self tolerance.

Project description:T cells proliferate vigorously following acute depletion of CD4+ Foxp3+ T regulatory cells [natural Tregs (nTregs)] and also when naive T cells are transferred to syngeneic, nTreg-deficient Rag1 -/- hosts. Here, using mice raised in an antigen-free (AF) environment, we show that proliferation in these two situations is directed to self ligands rather than food or commensal antigens. In both situations, the absence of nTregs elevates B7 expression on host dendritic cells (DCs) and enables a small subset of naive CD4 T cells with high self affinity to respond overtly to host DCs: bidirectional T/DC interaction ensues, leading to progressive DC activation and reciprocal strong proliferation of T cells accompanied by peripheral Treg (pTreg) formation. Likewise, high-affinity CD4 T cells proliferate vigorously and form pTregs when cultured with autologous DCs in vitro in the absence of nTregs: this anti-self response is MHCII/peptide dependent and elicited by the raised level of B7 on cultured DCs. The data support a model in which self tolerance is imposed via modulation of CD28 signaling and explains the pathological effects of superagonistic CD28 antibodies.

| S-EPMC6338877 | biostudies-literature

Thymic mimetic cells function beyond self-tolerance [scATAC-Seq Multiome]

Project description:Thymic mimetic cells function beyond self-tolerance [scATAC-Seq Multiome]

| PRJNA991998 | ENA

Thymic mimetic cells function beyond self-tolerance [IgM and Ccr6]

Project description:Thymic mimetic cells function beyond self-tolerance [IgM and Ccr6]

| PRJNA988545 | ENA

Msi1 integrates APC loss and mTORC1 activation to promote intestinal stem cell transformation

Project description:Loss of the APC tumor suppressor in the intestinal epithelium initiates the majority of human colorectal adenocarcinomas. Constitutive Î²-catenin activation is thought to underlie tumorigenesis induced by loss of APC, however Î²-catenin activation alone does not recapitulate all APC-loss phenotypes, suggesting that additional pathways are required. We demonstrate that aberrant activation of the Msi1 RNA binding protein occurs upon APC loss and that constitutive Msi1 activation alone is sufficient to phenocopy APC loss in the intestinal epithelium. Msi1 elicits these effects through binding of mRNAs encoding pleiotropic tumor suppressors resulting in promiscuous activation of quiescent intestinal stem cells, proliferative expansion of the stem cell compartment, crypt fission, and blocked differentiation. Further, we find these phenotypes to be largely dependent on mTORC1 activity, and demonstrate that loss of Msi activity is sufficient to abrogate tumorigenesis in mouse and human systems. Our findings implicate Msi1 as a central coordinator of APC loss-induced intestinal stem cell transformation and adenocarcinoma progression. 2 wild-type, 2 transgenic samples

2015-10-22 | E-GEOD-54598 | biostudies-arrayexpress

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