Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset
Heritable susceptibility of the autoimmune disorder, type 1 diabetes (T1D), only partially equates for the incidence of the disease. Significant evidence attributes several environmental stressors, such as vitamin D deficiency, gut microbiome, dietary antigens, and most notably virus infections in t...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2017-09-01
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| Series: | Frontiers in Endocrinology |
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| Online Access: | http://journal.frontiersin.org/article/10.3389/fendo.2017.00249/full |
| _version_ | 1818426987470913536 |
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| author | Zachary J. Morse Marc S. Horwitz |
| author_facet | Zachary J. Morse Marc S. Horwitz |
| author_sort | Zachary J. Morse |
| collection | DOAJ |
| description | Heritable susceptibility of the autoimmune disorder, type 1 diabetes (T1D), only partially equates for the incidence of the disease. Significant evidence attributes several environmental stressors, such as vitamin D deficiency, gut microbiome, dietary antigens, and most notably virus infections in triggering the onset of T1D in these genetically susceptible individuals. Extensive epidemiological and clinical studies have provided credibility to this causal relationship. Infection by the enterovirus, coxsackievirus B, has been closely associated with onset of T1D and is considered a significant etiological agent for disease induction. Recognition of viral antigens via innate pathogen-recognition receptors induce inflammatory events which contribute to autoreactivity of pancreatic self-antigens and ultimately the destruction of insulin-secreting beta cells. The activation of these specific innate pathways and expression of inflammatory molecules, including type I and III interferon, prime the immune system to elicit either a protective regulatory response or a diabetogenic effector response. Therefore, sensing of viral antigens by retinoic acid-inducible gene I-like receptors and toll-like receptors may be detrimental to inducing autoreactivity initiated by viral stress and resulting in T1D. |
| first_indexed | 2024-12-14T14:38:34Z |
| format | Article |
| id | doaj.art-d3af9d19f638425a9158c79ff366e6dc |
| institution | Directory Open Access Journal |
| issn | 1664-2392 |
| language | English |
| last_indexed | 2024-12-14T14:38:34Z |
| publishDate | 2017-09-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj.art-d3af9d19f638425a9158c79ff366e6dc2022-12-21T22:57:30ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922017-09-01810.3389/fendo.2017.00249295419Innate Viral Receptor Signaling Determines Type 1 Diabetes OnsetZachary J. Morse0Marc S. Horwitz1Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, CanadaDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, BC, CanadaHeritable susceptibility of the autoimmune disorder, type 1 diabetes (T1D), only partially equates for the incidence of the disease. Significant evidence attributes several environmental stressors, such as vitamin D deficiency, gut microbiome, dietary antigens, and most notably virus infections in triggering the onset of T1D in these genetically susceptible individuals. Extensive epidemiological and clinical studies have provided credibility to this causal relationship. Infection by the enterovirus, coxsackievirus B, has been closely associated with onset of T1D and is considered a significant etiological agent for disease induction. Recognition of viral antigens via innate pathogen-recognition receptors induce inflammatory events which contribute to autoreactivity of pancreatic self-antigens and ultimately the destruction of insulin-secreting beta cells. The activation of these specific innate pathways and expression of inflammatory molecules, including type I and III interferon, prime the immune system to elicit either a protective regulatory response or a diabetogenic effector response. Therefore, sensing of viral antigens by retinoic acid-inducible gene I-like receptors and toll-like receptors may be detrimental to inducing autoreactivity initiated by viral stress and resulting in T1D.http://journal.frontiersin.org/article/10.3389/fendo.2017.00249/fulltype 1 diabetesautoimmunityinnate immunitytoll-like receptorsRIG-I-like receptorsMDA5 |
| spellingShingle | Zachary J. Morse Marc S. Horwitz Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset Frontiers in Endocrinology type 1 diabetes autoimmunity innate immunity toll-like receptors RIG-I-like receptors MDA5 |
| title | Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset |
| title_full | Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset |
| title_fullStr | Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset |
| title_full_unstemmed | Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset |
| title_short | Innate Viral Receptor Signaling Determines Type 1 Diabetes Onset |
| title_sort | innate viral receptor signaling determines type 1 diabetes onset |
| topic | type 1 diabetes autoimmunity innate immunity toll-like receptors RIG-I-like receptors MDA5 |
| url | http://journal.frontiersin.org/article/10.3389/fendo.2017.00249/full |
| work_keys_str_mv | AT zacharyjmorse innateviralreceptorsignalingdeterminestype1diabetesonset AT marcshorwitz innateviralreceptorsignalingdeterminestype1diabetesonset |