Characterization of the humoral immune response to glutamic acid decarboxylase in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) and/or type 1 diabetes.
Characterization of the humoral immune response to glutamic acid decarboxylase in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) and/or type 1 diabetes.
复制标题
自身免疫性多内分泌病-念珠菌病-外胚层营养不良 (APECED) 和/或 1 型糖尿病患者对谷氨酸脱羧酶的体液免疫反应的特征。
DOI:
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复制
发表时间:
2005
影响因子:
5.8
通讯作者:
M. Knip
中科院分区:
文献类型:
--
作者:
M. Ronkainen;T. Härkönen;J. Perheentupa;M. Knip
OBJECTIVE
A humoral autoimmune response to glutamic acid decarboxylase (GAD65) is common both in patients with type 1 diabetes and in those with the autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome, while overt type 1 diabetes is relatively rarely diagnosed in APECED patients. The aim of this study was to assess whether this difference in the incidence of type 1 diabetes is associated with variability in the humoral immune response to GAD65, one of the major autoantigens in type 1 diabetes.
METHODS
Epitope- and isotype-specific GAD65 autoantibodies were analysed in 20 patients with APECED and 20 patients with newly diagnosed type 1 diabetes alone by radiobinding assays.
RESULTS
GAD65 autoantibodies targeted the middle and carboxy-terminal regions of GAD65 and occasionally the amino-terminal region in the APECED patients and comprised mainly the IgG1 subclass and less frequently the IgG2 and IgG4 subclasses. The profile of epitope- and isotype-specific GAD65 autoantibodies was similar in type 1 diabetes and APECED, except that IgG2 subclass antibodies were observed more often and at higher levels in the patients with type 1 diabetes alone (P < 0.05). None of the measured parameters separated APECED patients with type 1 diabetes from those without type 1 diabetes.
CONCLUSION
APECED-associated humoral autoimmunity to GAD65 does not differ markedly from that observed in type 1 diabetes; only IgG2-GAD65 antibodies may be more closely associated with the latter entity.
DOI:
10.1073/pnas.89.6.2115
发表时间:
1992-03-15
影响因子:
11.1
作者:
BU, DF;ERLANDER, MG;TOBIN, AJ
通讯作者:
TOBIN, AJ
DOI:
10.1210/jcem.81.4.8636356
发表时间:
1996
期刊:
The Journal of clinical endocrinology and metabolism
影响因子:
--
作者:
Tuomi,T;Björses,P;Falorni,A;Partanen,J;Perheentupa,J;Lernmark,A;Miettinen,A
通讯作者:
Miettinen,A