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The pancreas in human type 1 diabetes

Type 1 diabetes (T1D) is considered a disorder whose pathogenesis is autoimmune in origin, a notion drawn in large part from studies of human pancreata performed as far back as the 1960s. While studies of the genetics, epidemiology, and peripheral immunity in T1D have been subject to widespread anal...

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Detalles Bibliográficos
Autores principales: Rowe, Patrick A., Campbell-Thompson, Martha L., Schatz, Desmond A., Atkinson, Mark A.
Formato: Texto
Lenguaje:English
Publicado: Springer-Verlag 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022158/
https://www.ncbi.nlm.nih.gov/pubmed/20495921
http://dx.doi.org/10.1007/s00281-010-0208-x
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author Rowe, Patrick A.
Campbell-Thompson, Martha L.
Schatz, Desmond A.
Atkinson, Mark A.
author_facet Rowe, Patrick A.
Campbell-Thompson, Martha L.
Schatz, Desmond A.
Atkinson, Mark A.
author_sort Rowe, Patrick A.
collection PubMed
description Type 1 diabetes (T1D) is considered a disorder whose pathogenesis is autoimmune in origin, a notion drawn in large part from studies of human pancreata performed as far back as the 1960s. While studies of the genetics, epidemiology, and peripheral immunity in T1D have been subject to widespread analysis over the ensuing decades, efforts to understand the disorder through analysis of human pancreata have been far more limited. We have reviewed the published literature pertaining to the pathology of the human pancreas throughout all stages in the natural history of T1D. This effort uncovered a series of findings that challenge many dogmas ascribed to T1D and revealed data suggesting the marked heterogeneity in terms of its pathology. An improved understanding and appreciation for pancreatic pathology in T1D could lead to improved disease classification, an understanding of why the disorder occurs, and better therapies for disease prevention and management.
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spelling pubmed-30221582011-02-22 The pancreas in human type 1 diabetes Rowe, Patrick A. Campbell-Thompson, Martha L. Schatz, Desmond A. Atkinson, Mark A. Semin Immunopathol Review Type 1 diabetes (T1D) is considered a disorder whose pathogenesis is autoimmune in origin, a notion drawn in large part from studies of human pancreata performed as far back as the 1960s. While studies of the genetics, epidemiology, and peripheral immunity in T1D have been subject to widespread analysis over the ensuing decades, efforts to understand the disorder through analysis of human pancreata have been far more limited. We have reviewed the published literature pertaining to the pathology of the human pancreas throughout all stages in the natural history of T1D. This effort uncovered a series of findings that challenge many dogmas ascribed to T1D and revealed data suggesting the marked heterogeneity in terms of its pathology. An improved understanding and appreciation for pancreatic pathology in T1D could lead to improved disease classification, an understanding of why the disorder occurs, and better therapies for disease prevention and management. Springer-Verlag 2010-05-22 2011 /pmc/articles/PMC3022158/ /pubmed/20495921 http://dx.doi.org/10.1007/s00281-010-0208-x Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Review
Rowe, Patrick A.
Campbell-Thompson, Martha L.
Schatz, Desmond A.
Atkinson, Mark A.
The pancreas in human type 1 diabetes
title The pancreas in human type 1 diabetes
title_full The pancreas in human type 1 diabetes
title_fullStr The pancreas in human type 1 diabetes
title_full_unstemmed The pancreas in human type 1 diabetes
title_short The pancreas in human type 1 diabetes
title_sort pancreas in human type 1 diabetes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022158/
https://www.ncbi.nlm.nih.gov/pubmed/20495921
http://dx.doi.org/10.1007/s00281-010-0208-x
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