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Reduced function of the adaptor SH2B3 promotes T1D via altered gc cytokine-regulated, T cell intrinsic immune tolerance

ABSTRACT: Reduced function of the adaptor SH2B3 promotes T1D via altered gc cytokine-regulated, T cell intrinsic immune tolerance

PROVIDER: PRJNA1227910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32481100_1.fastq.gz	Fastqsanger.gz
	SRR32481100_2.fastq.gz	Fastqsanger.gz
	SRR32481101_1.fastq.gz	Fastqsanger.gz
	SRR32481101_2.fastq.gz	Fastqsanger.gz
	SRR32481102_1.fastq.gz	Fastqsanger.gz

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Reduced function of the adaptor SH2B3 promotes T1D via altered gc cytokine-regulated, T cell intrinsic immune tolerance

Project description:Genome-wide assocation studie have identified SH2B3 as an important non-MHC gene for islet autoimmunity and type 1 diabetes (T1D). In this study, we found a single haplotype strongly associated with risk for human T1D that includes the sinlge nucleotide variant rs3184505*T in SH2B3. To better characterize the role of SH2B3 in T1D, we used moouse modeling and found a T cell-intrisic role for SH2B3 regulating peripheral tolerance. SH2B3 deficiency had minimal effect on TCR signaling or. proliferation across antigen doses, yet enhance cell survival and cytokine signaling including common gamma chain-dependent and interferon-gamma receptor signaling. SH2B3 deficient CD8+T cells showed augmented STAT5-Myc and effector function gene expression partially reversed when blocking autocrine IL-2 in culture. Using the RIP-mOVA model, we found T cells lacking SH2B3 promoted early islet destruction and diasbetes without requiring CD4+ T cell help. SH2B3-deficient cells demontrated increased survival post-transfer compared to control cells despite a similar proliferation profile in the same host. Next we created a spontatneous NOD.Sh2b3-/- mouse model and found markedly increased incidence and accelerated T1D across genders. Collectively, these studies identify SH2B3 as a critical mediator of peripheral T cell tolerance lmiting the T cell response to self-antigens.

2025-02-27 | GSE290401 | GEO

m6A RIP-seq for Cytokine-treated Islets and Beta-cells or T1D Islets

Project description:m6A RIP-seq for Cytokine-treated Islets and Beta-cells or T1D Islets

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Project description:Type 1 Diabetes (T1D) is characterized by autoimmune-mediated destruction of insulin-producing beta-cells. Recent research has focused on the role of the innate immune system in initiating this process. To investigate this further, we used m6A-profiling of human islets from non-diabetic individuals and the human beta-cell line EndoC-bH1 treated with PBS or interleukin 1 beta and interferon alpha, as well as established T1D patients. Our findings reveal that N6-Methyladenosine (m6A) is a mechanism that helps protect beta-cells by accelerating the decay of mRNA from the 2'-5'-oligoadenylate synthetase (OAS) genes, which controls the antiviral innate immune response at the onset of T1D. These results provide insight into the adaptive safeguarding mechanisms of beta-cells and the role of m6A in T1D development, highlighting potential targets for therapeutic interventions.

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Expression data from recent-onset T1D patients and controls

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Project description:To unravel genes and molecular pathways involved in the pathogenesis of type 1 diabetes (T1D), we performed genome-wide gene expression profiling of prospective venous blood samples from children developing T1D-associated autoantibodies or progressing towards clinical diagnosis. 357 peripheral blood RNA samples from 10 autoantibody-positive children (Case) and their matched controls (Control) or alternatively 18 prediabetic children (T1DCase) and their matched controls (T1DControl) were analyzed with Affymetrix U219 gene array, in order to study the gene expression changes occuring during the pathogenesis of Type 1 diabetes (T1D). Each case child (positive for T1D-specific autoantibodies) was matched with a persistently autoantibody-negative control child, with the same HLA-DQB1 risk category, gender, and place and date of birth. Seroconversion is determined as the first detection of T1D-specific autoantibody/autoantibodies (ICA titre >4 JDFU, IAA >3.47 RU, GADA >5.4 RU, IA-2A >0.43 RU, ZnT8A >0.61 RU). Two control children were selected for T1D cases 3, 5, 13 and 17. Case5 & T1DCase15 and Case7 & T1DCase3 share the same matched control. Sample T1DControl7_4 was excluded from the final analysis as an outlier, resulting in 356 total Samples listed below.

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Project description:Naturally occurring FoxP3+CD4+CD25+high regulatory T cells (Tregs) play an important role in dominant tolerance, suppressing auto-reactive CD4+CD25- T cell activity. Although Tregs from T1D subjects are functionally deficient, there is little knowledge of the molecular mechanisms that orchestrate this loss of Treg function. We observed increased apoptosis (by a novel YOPRO-1/7AAD dual staining protocol) and decreased suppression in polyclonal Tregs in the periphery from high at-risk and T1D subjects. We hypothesize that prior to and during the onset of disease, Tregs lack pro-survival signals and are caught up in a relatively deficient cytokine milieu whose effects may be detectable in the periphery. Microarray analysis was performed on un-stimulated Tregs from 12 subjects with newly diagnosed T1D and 15 healthy controls. Experiment Overall Design: Recent-onset T1D subjects were T1D patients diagnosed within 1 year. At the time of each visit, the following clinical measurements were taken: HbA1c, glucose level, height, weight and BMI. The presence of auto-antibodies was measured from peripheral blood. Peripheral blood mononuclear cells (PBMCs) were collected and Tregs were isolated using FACS isolation. RNA was isolated, amplified and cRNA was fragmented and hybridized to Affymetrix whole genome U133Plus2.0 arrays having 54675 probe-sets. Bayesian Hierarchical analysis (BGX) was used to analyze the data.

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