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Potential viral pathogenic mechanism in human type 1 diabetes

In type 1 diabetes, as a result of as yet unknown triggering events, auto-aggressive CD8(+) T cells, together with a significant number of other inflammatory cells, including CD8(+) T lymphocytes with unknown specificity, infiltrate the pancreas, leading to insulitis and destruction of the insulin-p...

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Detalles Bibliográficos
Autores principales: Schneider, Darius A., von Herrath, Matthias G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4153966/
https://www.ncbi.nlm.nih.gov/pubmed/25073445
http://dx.doi.org/10.1007/s00125-014-3340-7
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author Schneider, Darius A.
von Herrath, Matthias G.
author_facet Schneider, Darius A.
von Herrath, Matthias G.
author_sort Schneider, Darius A.
collection PubMed
description In type 1 diabetes, as a result of as yet unknown triggering events, auto-aggressive CD8(+) T cells, together with a significant number of other inflammatory cells, including CD8(+) T lymphocytes with unknown specificity, infiltrate the pancreas, leading to insulitis and destruction of the insulin-producing beta cells. Type 1 diabetes is a multifactorial disease caused by an interactive combination of genetic and environmental factors. Viruses are major environmental candidates with known potential effects on specific key points in the pathogenesis of type 1 diabetes and recent findings seem to confirm this presumption. However, we still lack well-grounded mechanistic explanations for how exactly viruses may influence type 1 diabetes aetiology. In this review we provide a summary of experimentally defined viral mechanisms potentially involved in the ontology of type 1 diabetes and discuss some novel hypotheses of how viruses may affect the initiation and natural history of the disease.
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spelling pubmed-41539662014-09-04 Potential viral pathogenic mechanism in human type 1 diabetes Schneider, Darius A. von Herrath, Matthias G. Diabetologia Review In type 1 diabetes, as a result of as yet unknown triggering events, auto-aggressive CD8(+) T cells, together with a significant number of other inflammatory cells, including CD8(+) T lymphocytes with unknown specificity, infiltrate the pancreas, leading to insulitis and destruction of the insulin-producing beta cells. Type 1 diabetes is a multifactorial disease caused by an interactive combination of genetic and environmental factors. Viruses are major environmental candidates with known potential effects on specific key points in the pathogenesis of type 1 diabetes and recent findings seem to confirm this presumption. However, we still lack well-grounded mechanistic explanations for how exactly viruses may influence type 1 diabetes aetiology. In this review we provide a summary of experimentally defined viral mechanisms potentially involved in the ontology of type 1 diabetes and discuss some novel hypotheses of how viruses may affect the initiation and natural history of the disease. Springer Berlin Heidelberg 2014-07-30 2014 /pmc/articles/PMC4153966/ /pubmed/25073445 http://dx.doi.org/10.1007/s00125-014-3340-7 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Review
Schneider, Darius A.
von Herrath, Matthias G.
Potential viral pathogenic mechanism in human type 1 diabetes
title Potential viral pathogenic mechanism in human type 1 diabetes
title_full Potential viral pathogenic mechanism in human type 1 diabetes
title_fullStr Potential viral pathogenic mechanism in human type 1 diabetes
title_full_unstemmed Potential viral pathogenic mechanism in human type 1 diabetes
title_short Potential viral pathogenic mechanism in human type 1 diabetes
title_sort potential viral pathogenic mechanism in human type 1 diabetes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4153966/
https://www.ncbi.nlm.nih.gov/pubmed/25073445
http://dx.doi.org/10.1007/s00125-014-3340-7
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