Potential role of type I interferon in the pathogenic process leading to type 1 diabetes
| Autor: | Jennifer P. Wang, Agata Jurczyk, Natasha Qaisar |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
endocrine system endocrine system diseases Endocrinology Diabetes and Metabolism Apoptosis Autoimmunity Inflammation Biology Major histocompatibility complex medicine.disease_cause Article Proinflammatory cytokine Islets of Langerhans 03 medical and health sciences Endocrinology Interferon Insulin-Secreting Cells Internal Medicine medicine Animals Humans Nutrition and Dietetics Innate immune system Gene signature Immunity Innate Diabetes Mellitus Type 1 030104 developmental biology Interferon Type I Immunology biology.protein Signal transduction medicine.symptom Signal Transduction medicine.drug |
| Zdroj: | Current Opinion in Endocrinology & Diabetes and Obesity. 25:94-100 |
| ISSN: | 1752-296X |
| Popis: | PURPOSE: Understanding the relationship between viral infections and the development of type 1 diabetes (T1D) are essential for T1D prevention. Virus-induced innate immune responses, specifically type I interferon (IFN-I) and the IFN gene signature, orchestrate early events of β- cell dysfunction preceding islet autoimmunity. We summarize recent advances in how IFN-I and the IFN gene signature can drive T1D development. RECENT FINDINGS: IFN-I, particularly interferon-alpha (IFN-α), and the IFN gene signature have been detected in islets and peripheral blood of T1D patients. T1D risk genes in the IFN-I signaling pathway regulate antiviral responses in β-cells driven by IFN-I and proinflammatory cytokines. Polymorphisms in these genes may cause chronic dysregulated IFN signaling in islets, characterized by hyperexpression of IFN-I, the IFN gene signature and major histocompatibility complex (MHC) class I during viral infection. Islet cell inflammation mediated by aberrant IFN signaling drives β-cell apoptosis by initiating autoreactivity against β-cell antigens. The profound elevation in IFN-I and the IFN gene signature observed in some forms of T1D are also seen in a novel group of human autoimmune and autoinflammatory diseases called interferonopathies. SUMMARY: Despite significant advances, further studies are required to functionally dissect the mechanisms by which excessive IFN-I contributes to the evolution of autoimmunity that destroys β-cells. |
| Databáze: | OpenAIRE |
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