Characterization of human organ donors testing positive for type 1 diabetes-associated autoantibodies
2015 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 182, no 3, 278-288 p.Article in journal (Refereed) Published
In this study we aim to describe the characteristics of non-diabetic organ donors with circulating diabetes-associated autoantibodies collected within the Nordic Network for Islet Transplantation. One thousand and thirty organ donors have been screened in Uppsala for antibodies against glutamic acid decarboxylase (GADA) and islet antigen-2 (IA-2A). The 32 non-diabetic donors that tested positive for GADA (33% of all non-diabetic donors) were studied in more detail, together with 32 matched controls. Mean age among the autoantibody-positive donors was 526 (range 21-74), family history of type 1 diabetes (T1D) was unknown, and no donor was genetically predisposed for T1D regarding the human leucocyte antigen (HLA) locus. Subjects were analysed for islet cell antibodies (ICA), insulin autoantibodies (IAA) and zinc transporter 8 antibodies (ZnT8A), and pancreas morphology and clinical data were examined. Eight non-diabetic donors tested positive for two antibodies and one donor tested positive for four antibodies. No insulitis or other signs of a diabetic process were found in any of the donors. While inflammatory cells were present in all donors, subjects with high GADA titres had significantly higher CD45 cell numbers in exocrine tissue than controls. The extent of fibrosis was more pronounced in autoantibody-positive donors, even in subjects with lower GADA titres. Notably, it is possible that events not related directly to T1D (e.g. subclinical pancreatitis) may induce autoantibodies in some cases.
Place, publisher, year, edition, pages
2015. Vol. 182, no 3, 278-288 p.
autoantibodies, exocrine pancreas, fibrosis, inflammation, type 1 diabetes
Immunology in the medical area Other Basic Medicine
IdentifiersURN: urn:nbn:se:uu:diva-268390DOI: 10.1111/cei.12698ISI: 000364235000005PubMedID: 26313035OAI: oai:DiVA.org:uu-268390DiVA: diva2:878659
FunderSwedish Research Council, 65X-12219-15-6Swedish Research Council, K2015-54X-12219-19-4EU, FP7, Seventh Framework Programme, PEVNET 261441Novo NordiskSwedish Diabetes AssociationSwedish Child Diabetes Foundation