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No Evidence for Presence of Mucosal-Associated Invariant T Cells in the Insulitic Lesions in Patients Recently Diagnosed with Type 1 Diabetes
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Oslo Univ Hosp, Div Paediat & Adolescent Med, Oslo, Norway.;Univ Oslo, Fac Odontol, Oslo, Norway..
Oslo Univ Hosp, Dept Endocrinol, Oslo, Norway.;Univ Oslo, Fac Med, Oslo, Norway..
Oslo Univ Hosp, Div Paediat & Adolescent Med, Oslo, Norway.;Univ Oslo, Fac Med, Oslo, Norway..
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2018 (English)In: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Vol. 188, no 8, p. 1744-1748Article in journal (Refereed) Published
Abstract [en]

Mucosal-associated invariant T (MAIT) cells are innate T cells that recognize bacteria-infected cells and are thought to play a role in autoimmune diseases. Translocation of duodenal bacteria and viruses to the pancreas through the pancreatic duct has been hypothesized to initiate an innate inflammatory response that could contribute to the development of type 1 diabetes, a process that could involve MAIT cells. In this study, we used immunohistochemistry and quantitative PCR to search for evidence of MAIT cells in the insulitic lesions in the pancreas of human patients recently diagnosed with type 1 diabetes. Only a few scattered MAIT cells were found within the exocrine parenchyma in all pancreatic samples, but no MAIT cells were found in association to the islets. Also, only low gene expression levels of the MAIT T-cell receptor V alpha 7.2-3 alpha 33 were found in the pancreas of patients with type 1 diabetes, in similar Levels as that in nondiabetic organ donors used as control. The absence of MAIT cells shown in insulitic lesions in humans questions the direct cytotoxic role of these cells in beta-cell destruction.

Place, publisher, year, edition, pages
Elsevier, 2018. Vol. 188, no 8, p. 1744-1748
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-364915DOI: 10.1016/j.ajpath.2018.04.009ISI: 000440773100002PubMedID: 29803829OAI: oai:DiVA.org:uu-364915DiVA, id: diva2:1261830
Funder
Swedish Research Council, 65X-12219-15-6 K'2015-54X-12219-19-4Novo NordiskÅke Wiberg FoundationTore Nilsons Stiftelse för medicinsk forskningSwedish Child Diabetes FoundationSwedish Diabetes AssociationEU, FP7, Seventh Framework Programme, 26441 PEVNETAvailable from: 2018-11-08 Created: 2018-11-08 Last updated: 2018-11-08Bibliographically approved

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Kuric, EnidaSkog, OskarKorsgren, Olle

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