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Revisiting the notion of type 1 diabetes being a T-cell-mediated autoimmune disease
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Microbiology and Infectious Medicine, Clinical Bacteriology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
2013 (English)In: Current Opinion In Endocrinology Diabetes And Obesity, ISSN 1752-296X, Vol. 20, no 2, 118-123 p.Article, review/survey (Refereed) Published
Abstract [en]

Purpose of review Type 1 diabetes (T1D) research is at present in a critical period of development and during the past few years several large phase III studies targeting T-cell autoimmunity in recent-onset patients with T1D failed to reach the primary endpoint. Recent findings Cause and pathogenesis of T1D remain largely unknown. In humans, insulitis is discrete, affects few islets and is present only in about one-third of patients with recent-onset T1D. The rapid increase in incidence of T1D argues against a decisive role for genetic factors and instead for the hypothesis that infectious agents, possibly entering the pancreas via the ductal compartment, are involved in disease pathogenesis. Repeated episodes of bacteria or virus-induced innate inflammations affecting only certain lobes of the pancreas fit well with the reported heterogeneity of the disease within the pancreas as well as with the slow progression over many years. Summary In humans there is limited support for T1D being primarily an autoimmune disease; instead available findings support the view that T1D can be regarded as an innate inflammatory disease affecting the entire pancreas, but with its main clinical manifestations emanating from the loss of the insulin-producing cells.

Place, publisher, year, edition, pages
2013. Vol. 20, no 2, 118-123 p.
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-197756DOI: 10.1097/MED.0b013e32835edb89ISI: 000315479900006OAI: oai:DiVA.org:uu-197756DiVA: diva2:614069
Available from: 2013-04-03 Created: 2013-04-03 Last updated: 2013-04-03Bibliographically approved

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Skog, OskarMelhus, ÅsaKorsgren, Olle

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