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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

ABSTRACT: Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

PROVIDER: PRJNA1137917 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29891851_1.fastq.gz	Fastqsanger.gz
	SRR29891851_2.fastq.gz	Fastqsanger.gz
	SRR29891852_1.fastq.gz	Fastqsanger.gz
	SRR29891852_2.fastq.gz	Fastqsanger.gz
	SRR29891853_1.fastq.gz	Fastqsanger.gz

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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

Project description:Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (whole genome enzymatic methylation sequencing)

Project description:Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (whole genome enzymatic methylation sequencing)

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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation

Project description:The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.

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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (NOD)

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Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation (whole genome enzymatic methylation sequencing)

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Canagliflozin impairs T-cell effector function via metabolic suppression in autoimmunity [Autoimmune Profiling]

Project description:Augmented T-cell function leading to host damage in autoimmunity is supported by metabolic dysregulation. Targeting immunometabolism for the treatment of autoimmunity by repurposing clinically approved metabolic modulators, such as those used to treat people with type 2 diabetes (T2D), is therefore an attractive avenue. Canagliflozin, a class of the newest type of T2D drug – sodium glucose co-transporter 2 (SGLT2) inhibitors – has known off-target effects including mitochondrial glutamate dehydrogenase (GDH) and complex I inhibition. To date, the effects of SGLT2 inhibitors on human T-cell function are extremely limited. Here, we analysed 784 genes using the Nanostring nCounter® Autoimmune Profiling Panel and discovered 42 genes that were differentially regulated between canagliflozin-treated (cana, C; n = 6) and DMSO vehicle control (V; n = 6) T-cells. Of these genes, 39 were downregulated, including IL2, CSF2 and CCL20; whilst 3 were upregulated, including SELL. Dapagliflozin was used as another control, as this SGLT2 inhibitor does not exhibit any known off-target effects like canagliflozin. Here, there were no differentially expressed genes between dapagliflozin-treated (dapa, D; n = 4) and DMSO vehicle control (V; n = 4) T-cells. These analyses allowed a greater understanding of the global changes in T-cell function that occur in response to treatment with SGLT2 inhibitors.

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Sex Bias in CNS Autoimmune Disease Mediated by Androgen Control of Autoimmune Regulator

Project description:Male gender is protective against multiple sclerosis and other T cell-mediated autoimmune diseases. This protection may be due, in part, to higher androgen levels in males. Androgen binds to the androgen receptor (AR) to regulate gene expression, but how androgen protects against autoimmunity is not well-understood. Autoimmune Regulator (Aire) prevents autoimmunity by promoting self-antigen expression in medullary thymic epithelial cells, such that developing T cells that recognize these self-antigens within the thymus undergo clonal deletion. Here, we show that androgen upregulates Aire-mediated thymic tolerance to protect against autoimmunity. Androgen recruits AR to Aire promoter regions, with consequent enhancement of Aire transcription. In mice and humans, thymic Aire expression is higher in males compared to females. Androgen administration and male gender protect against autoimmunity in a multiple sclerosis mouse model in an Aire-dependent manner. Thus, androgen control of an intrathymic Aire-mediated tolerance mechanism contributes to gender differences in autoimmunity. RNA-seq comparison of male vs. female expression in mTEC cells. Pools of 10 mice each were used for each replicate (two for male and two for female)

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Project description:The gastrointestinal ecosystem is a highly complex environment with a profound influence on human health. Inflammation in the gut, linked to an altered gut microbiome has been associated with the development of multiple human conditions including type 1 diabetes (T1D). Viruses infecting the gastrointestinal tract, especially enteroviruses, are also thought to play an important role in T1D pathogenesis possibly via overlapping mechanisms. Here, we apply an integrative approach to combine comprehensive faecal virome, microbiome and metaproteome data sampled before and at the onset of islet autoimmunity in 40 children. We show strong age and antibody related effects across the datasets. Mastadenovirus infection was associated with profound functional changes in the faecal metaproteome. Multiomic factor analysis modelling revealed proteins associated with carbohydrate transport from the genus Faecalibacterium were associated with islet autoimmunity. These findings demonstrate functional remodelling of the gut microbiota accompanies both islet autoimmunity and viral infection.

2022-08-22 | PXD032997 | Pride

Lack of AtMC1 catalytic activity triggers autoimmunity dependent on NLR stability

Project description:Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Although individual mutations in NLRs, PRRs or other immune-related components that interact with catalytically inactive AtMC1 do not rescue the autoimmune phenotype, overexpression of SNIPER1, a master regulator of NLR homeostasis, fully attenuates the phenotype, inferring that a broad defect in NLR turnover may underlie the severe autoimmunity observed. As opposed to Wt AtMC1 which exhibits a nucleocytoplasmic localization, catalytically inactive AtMC1 localizes to puncta structures that are degraded through autophagy. We infer that the phenotypes observed in plants overexpressing catalytically inactive AtMC1 may represent an additive phenotype to the relatively milder autoimmunity observed in atmc1 mutants. Altogether and considering previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels as plants approach adulthood, thus preventing autoimmunity.

2025-03-21 | PXD048924 | Pride

The transcription factors ZEB2 and T-bet cooperate to program cytotoxic T cell terminal differentiation

Project description:T-bet is critical for cytotoxic T lymphocyte (CTL) differentiation, but it is unclear how it operates in a graded manner in the formation of both terminal effector and memory precursor cells during infection. We find that at high concentrations T-bet induced expression of Zeb2 mRNA, which then triggered CTLs to adopt terminally differentiated states. ZEB2 and T-bet cooperate to switch on a terminal CTL differentiation program, while simultaneously repressing genes necessary for central memory CTL development. Chromatin immunoprecipitation sequencing (ChIP-seq) showed that a large proportion of these genes were bound by T-bet, and this binding was altered by ZEB2 deficiency. Furthermore, T-bet overexpression could not fully bypass ZEB2 function. Thus, the coordinated actions of T-bet and ZEB2 outline a novel genetic pathway that forces commitment of CTLs to terminal differentiation, thereby restricting their memory cell potential. Splenocyte derived CD8+ T cells from C57BL/6 mice with either a wildtype (WT) (GzmB-Cre Zeb2+/+) or GzmB-Cre Zeb2-fl/fl (Zeb2-/-) backgrounds, following 8 days post infection with LCMV-Armstrong, were subsetted into KLRG1-hi/IL-7R-lo populations (terminal effectors, TE) or KLRG1-lo/IL-7R-hi (memory precursors, MP) populations. Four experimental groups, each with 3 samples, comprised of TE+WT, MP+WT, TE+ZEB2-/-, and MP+ZEB2-/-, were profiled for gene expression utilizing a polyA RNA prep and hybridized to the Illumina microarray platform IlluminaWG-v2.0.

2015-09-15 | E-GEOD-72408 | biostudies-arrayexpress

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