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Inflammatory islet damage in patients bearing HLA-DR 3 and/or DR 4 haplotypes does not lead to islet autoimmunity.
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- Additional Information
- Source:
Publisher: Springer Verlag Country of Publication: Germany NLM ID: 0006777 Publication Model: Print Cited Medium: Print ISSN: 0012-186X (Print) Linking ISSN: 0012186X NLM ISO Abbreviation: Diabetologia Subsets: MEDLINE
- Publication Information:
Original Publication: Berlin Springer Verlag
- Subject Terms:
- Abstract:
The hypothesis was tested that islet autoimmunity is induced by ongoing islet cell destruction in subjects with susceptibility genes HLA-DR 3 and/or DR 4. Sixty-one patients with confirmed chronic pancreatitis were analysed, 30 of whom expressed HLA-DR 3 and/or DR 4. Electron microscopy studies in 10 patients showed that the inflammatory process also affected islets, as recognisable from islet cell lysis, intrainsular fibrosis and immune cell infiltrates. None of the sera tested contained any of three markers of islet autoimmunity, ICA, IAA or GAD antibodies. A correlation was seen between the loss of exocrine function, as determined by the ALTAB-test, and of beta-cell function, as determined by the C-peptide response to i.v. glucagon. However, there was no preferential loss of beta-cell function in patients with HLA-DR 3 and/or DR 4. We conclude that islet cell destruction occurs during chronic pancreatitis, but does not trigger islet autoimmunity, even in the presence of HLA-DR 3 and/or DR 4.
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- Accession Number:
0 (Autoantibodies)
0 (Biomarkers)
0 (HLA-DR3 Antigen)
0 (HLA-DR4 Antigen)
0 (Insulin)
0 (Insulin Antibodies)
0 (islet cell antibody)
- Publication Date:
Date Created: 19940501 Date Completed: 19940912 Latest Revision: 20190816
- Publication Date:
20221213
- Accession Number:
10.1007/s001250050134
- Accession Number:
8056184
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