INFLAMMATORY ISLET DAMAGE IN PATIENTS BEARING HLA-DR 3-HAPLOTYPE AND/OR DR 4-HAPLOTYPE DOES NOT LEAD TO ISLET AUTOIMMUNITY

被引:11
作者
LAMPETER, EF
SEIFERT, I
LOHMANN, D
HEISE, JW
BERTRAMS, J
CHRISTIE, MR
KOLBBACHOFEN, V
KOLB, H
机构
[1] CITY HOSP,LEIPZIG,GERMANY
[2] UNIV DUSSELDORF,DEPT SURG,DUSSELDORF,GERMANY
[3] ELISABETH HOSP,DEPT LAB MED,ESSEN,GERMANY
[4] JOHN RADCLIFFE HOSP,NUFFIELD DEPT CLIN BIOCHEM,OXFORD OX3 9DU,ENGLAND
[5] UNIV DUSSELDORF,DEPT IMMUNOL,W-4000 DUSSELDORF,GERMANY
关键词
IDDM; CHRONIC PANCREATITIS; ISLET CELL ANTIBODIES; AUTOIMMUNITY;
D O I
10.1007/s001250050134
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
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页码:471 / 475
页数:5
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