Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice

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Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice

Both animal model and human studies indicate that commensal bacteria may modify type 1 diabetes (T1D) development. However, the underlying mechanisms by which gut microbes could trigger or protect from diabetes are not fully understood, especially the interaction of commensal bacteria with pathogenic CD8 T cells. In this study, using islet-specific glucose-6-phosphatase catalytic subunit-relate...

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Beta cells cannot directly prime diabetogenic CD8 T cells in nonobese diabetic mice.

Type 1 diabetes (T1D) is caused by the destruction of insulin-producing islet beta cells. CD8 T cells are prevalent in the islets of T1D patients and are the major effectors of beta cell destruction in nonobese diabetic (NOD) mice. In addition to their critical involvement in the late stages of diabetes, CD8 T cells are implicated in the initiation of disease. NOD mice, in which the beta2-micro...

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Autoreactive diabetogenic T-cells in NOD mice can efficiently expand from a greatly reduced precursor pool.

A broad repertoire of pancreatic beta-cell autoreactive T-cells normally contributes to the development of type 1 diabetes in NOD mice. However, it has been unknown if a large reduction in the precursor pool from which autoreactive T-cells are drawn would inhibit the development of type 1 diabetes. To address this issue, we reduced the precursor frequency of autoreactive T-cells in NOD mice thr...

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Idd9/11 Genetic Locus Regulates Diabetogenic Activity of CD4 T-Cells in Nonobese Diabetic (NOD) Mice

OBJECTIVE Although the H2(g7) major histocompatibility complex (MHC) provides the primary pathogenic component, the development of T-cell-mediated autoimmune type 1 diabetes in NOD mice also requires contributions from other susceptibility (Idd) genes. Despite sharing the H2(g7) MHC, the closely NOD-related NOR strain remains type 1 diabetes resistant because of contributions of protective Idd5...

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Islet Amyloid Polypeptide is not a Target Antigen for CD8+ T-Cells in Type 2 Diabetes

Background: Type 2 diabetes (T2D) is a chronic metabolic disorder in which beta-cells are destroyed. The islet amyloid polypeptide (IAPP) produced by beta-cells has been reported to influence beta-cell destruction. Objective: To evaluate if IAPP can act as an autoantigen and therefore, to see if CD8 + T-cells specific for this protein might be present in T2D patients. Methods: Peripheral blood ...

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ژورنال

عنوان ژورنال: Journal of Experimental Medicine

سال: 2016

ISSN: 0022-1007,1540-9538

DOI: 10.1084/jem.20160526