Humoral autoimmune responses to glutamic acid decarboxylase have similar target epitopes and subclass that show titer-dependent disease association

被引：23
作者：
Piquer, S
Belloni, C
Lampasona, V
Bazzigaluppi, E
Vianello, M
Giometto, B
Bosi, E
Bottazzo, GF
Bonifacio, E
机构：
[1] San Raffaele Sci Inst, Immunol Diabet Unit, I-20132 Milan, Italy
[2] San Raffaele Sci Inst, Dept Lab Med, I-20132 Milan, Italy
[3] Univ Padua, Dept Neurol & Psychiat Sci, Neurol Clin 2, I-35100 Padua, Italy
[4] Osped Pediat Bambino Gesu, Autoimmun & Immunogenet Labs, Rome, Italy
[5] Univ Barcelona, Hosp Clin, Inst Invest Biomed August Pi & Sunyer, Endocrinol & Diabet Unit, Barcelona, Spain
来源：
CLINICAL IMMUNOLOGY | 2005年 / 117卷 / 01期
关键词：
GAD antibodies; GAD epitopes; IgG subclasses; stiff man syndrome; type; 1; diabetes;
D O I：
10.1016/j.clim.2005.06.009
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Glutamic acid decarboxylase (GAD) is an autoantigen in stiff man syndrome (SMS) and type 1 diabetes (TIDM). Different GAD autoantibody characteristics in these disorders have suggested distinct underlying mechanisms of autoimmunity. Here, it is shown that increased prevalence of autoantibodies to GAD65 amino terminal and GAD67 epitopes and autoantibodies of IgG2, IgG3, or IgG4 subclass in patients with SMS (P < 0.001 vs. TIDM) are secondary to the markedly higher autoantibody titers in SMS patients (P < 0.0001) and that autoantibody epitopes and subclasses were similar when patients were matched for autoantibody titer. Exposure to autoantigen in the disorders is likely to involve similar Immoral antigenic determinants, but different B cell regulation. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码：31 / 35
页数：5
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