The ABBOS-peptide from bovine serum albumin causes an IFN-γ and IL-4 mRNA response in lymphocytes from children with recent onset of type 1 diabetes

被引:17
作者
Karlsson, MGE [1 ]
Ludvigsson, J
机构
[1] Linkoping Univ, Fac Hlth Sci, Dept Hlth & Environm, Div Pediat, S-58185 Linkoping, Sweden
[2] Linkoping Univ, Fac Hlth Sci, Clin Res Ctr, S-58185 Linkoping, Sweden
关键词
ABBOS; IFN-gamma; IL-4; type; 1; diabetes; Th-lymphocytes;
D O I
10.1016/S0168-8227(99)00127-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The ABBOS-peptide from bovine serum albumin (BSA) in cow's milk has been suggested to initiate the autoimmune process against the p-cells leading to type 1 diabetes. The aim of this study was to elucidate if the ABBOS-peptide is a possible trigger of type 1 diabetes. The cytokines IL-4 and IFN-gamma were determined at the level of transcription as mRNA in lymphocytes, stimulated with the ABBOS-peptide. Sixteen children with newly diagnosed type 1 diabetes were compared with 10 healthy controls matched for the diabetes associated HLA-type DR3/4. Antibodies to bovine serum albumin (BSA), insulin antibodies (IA), and antibodies against islet cells (ICA) were determined, as well as serum C-peptide. Increased mRNA expression for IFN-gamma and/or IL-4 could be observed in lymphocytes from 13/16 children with recent onset of diabetes after in vitro stimulation with the ABBOS-peptide. Low expression of IFN-gamma mRNA was associated with high secretion of C-peptide, whereas a positive relationship could be observed between expression of IL-4 mRNA and insulin antibodies. Expression of IFN-gamma and/or IL-4 mRNA was also detected in lymphocytes from 6/10 healthy controls. ABBOS may have a role as a reactive epitope in the upregulation of the autoimmune process against the p-cells but ABBOS does not seem to cause any specific Th1 response. An increased mRNA expression could also be seen in lymphocytes from healthy controls. Thus, the ABBOS-peptide might just cause or reflect an unspecific immune activity. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:199 / 207
页数:9
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