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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [RNA-seq]

ABSTRACT: We generated expression profiles of TH1 and TREG cells from T1D and healthy subjects by RNA-Seq. By integrating RNA-Seq dta with other data sets, we predicted and validated serveral T1D risk SNPs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE112341 | GEO | 2019/03/26

REPOSITORIES: GEO

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes [ChIP-seq]

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes

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Novel risk variants affecting enhancers of TH1 and TREG cells in type 1 diabetes

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Project description:We performed a comparison of transcriptome between monocyte-derived dendritic cells (moDC) cultured with neutrophil extracellular traps (NETs) from healthy donors or type 1 diabetes (T1D) patients. The source of moDCs is healthy donors and T1D patients

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Project description:Type 1 Diabetes (T1D) is considered to be a Th1 autoimmune disease characterised by an absolute lack of insulin caused by an autoimmune destruction of the insulin producing pancreatic beta cells. Th1 lymphocytes are responsible for the infiltration of the islets of Langerhans and for the cytokine release that supports cytotoxic (Tc) lymphocytes to mediate destruction of the beta cells. The preclinical disease stage is characterized by the generation of the self-reactive lymphocytes that infiltrate the pancreas and selectively destroy the insulin-producing beta cells present in the islets. Other cellular immune mechanisms regarding immunoregulation and antigen presentation and processing are involved in T1D pathogenesis as well. Our aim was to identify genes involved in the corresponding signalling cascades, especially those which may serve as promising diagnostic tools for the identification of persons in the prediabetic phase of the disease. We addressed the question by analysing gene expression profiles of freshly isolated peripheral blood mononuclear cells in type 1 diabetes patients, their first degree relatives divided according to their autoantibody status, and healthy controls. 9 T1D-patients versus 10 first degree relatives versus 10 healthy controls

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CXCR3+ Treg cells suppress Th1-immune responses through expression of the co-inhibitory receptors CD85k and Lag-3

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Project description:CD4 T cells were activated using CD3/CD28 antibodies in the presence of IL2 and IL12, to generate Th1 cells. Th1 cells were maintained and expanded in IL2 and IL12, on D5 Th1 cells were sorted for CD4+ expression and DAP1 exclusion. After flow sorting, live TH1 cells were resuspended (1e6 per ml) in methionine free RPMI, supplemented with 10% dialysed FBS, IL2 and IL12, and with L-methionine (100μM, or 1μM). Cells were cultured for 5 hrs before collection for proteomics processing.

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