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Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes (Mouse)

ABSTRACT: Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes (Mouse)

PROVIDER: PRJNA704315 | ENA |

REPOSITORIES: ENA

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Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes

Project description:Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes

| PRJNA704027 | ENA

Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes

Project description:Ex-vivo pharmacological modulation enhances the immunoregulatory and trafficking properties of HSCs which mitigated autoimmune diabetes and other autoimmune disorders. We used GeneChip microarrays to compare the whole transcriptomes of vehicle (DMSO) and dmPGE2 (10uM) + Dexamenthasone (uM) modulated human CD34+ HSPCs.

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Pharmacologically enhanced regulatory hematopoietic stem cells (HSC.Regs) reverts experimental autoimmune diabetes (Mouse)

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Transcription profiling of monocytes from patients with autoimmune diabetes

Project description:Identifying a discriminating expression pattern of inflammatory genes in monocytes of patients with autoimmune diabetes

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Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression

Project description:Whole population RNASeq of pancreatic islet macrophages during autoimmune diabetes progression.

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Analysis of a non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE)

Project description:The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. To achieve this, pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stages in the lesion. In the chronic phase of the NOD-EAE mice, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. We describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase.

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Lymphocyte Activation Gene-3 limits regulatory T cell proliferation and function in autoimmune diabetes

Project description:Inhibitory receptors (Irs) are pivotal in controlling T cell homeostasis because of their intrinsic regulation of conventional T (Tconv) cell proliferation, viability and function. However, the role of Irs on regulatory T (Treg) cells remains obscure, as they could be required for suppressive activity and/or limit Treg cell function. We evaluated the role of Lymphocyte Activation Gene-3 (LAG3, CD223) on Treg cells by generating mice in which LAG3 is absent on the cell surface of Treg cells in a murine model of Type 1 Diabetes. Surprisingly, mice that lacked LAG3 expression on Treg cells exhibited reduced autoimmune diabetes, consistent with enhanced Treg cell proliferation and function. Whereas the transcriptional landscape of peripheral wild-type (WT) and Lag3-deficient Treg cells was largely comparable, substantial differences between intra-islet Treg cells were evident and involved a subset of genes and pathways that promote Treg cell maintenance and function. Consistent with these observations, Lag3-deficient Treg cells out-competed WT Treg cells in the islets but not in the periphery in co-transfer experiments due to enhanced IL2-Stat5 signaling and Eos expression. Our study suggests that LAG3 intrinsically limits Treg cell proliferation and function at inflamed pancreas, promotes autoimmunity in a chronic autoimmune-prone environment and may contribute to Treg cell insufficiency in autoimmune disease

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Innate immunity-driven cell recruitment in rat autoimmune diabetes

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The mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes

Project description:Mitochondria are principal metabolic organelles that are increasingly unveiled as immune regulators. However, it is currently not known whether mitochondrial-encoded peptides modulate T cells to induce changes in phenotype and function. Here, we found that MOTS-c prevented autoimmune β-cell destruction via phenotypical and functional changes of T cells in NOD mice, a type 1 diabetes (T1D) animal model. MOTS-c ameliorated the development of hyperglycemia and reduced islet-infiltrating immune cells. Furthermore, adoptive transfer of T cells from MOTS-c-treated NOD mice significantly decreased the incidence of diabetes in NOD-SCID mice. Metabolic and genomic analysis revealed that MOTS-c modulated T cell phenotype and function by regulating TCR/mTORC1 pathway. We observed that T1D patients had a lower serum MOTS-c level than healthy controls. Furthermore, MOTS-c reduced T cell activation by alleviating T cells from the glycolytic stress in T1D patients suggesting a potential therapeutic implication. Our findings indicate that the MOTS-c acts as a regulator of T cell phenotype and function in autoimmune diabetes.

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Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire

Project description:We examined the transcriotional changes in antigen specific CD4 T cells to antigens derived from thymus or to the antigens derived from islets in the autoimmune diabetes mouse model.

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