Identification of autoantibody-negative autoimmune type 2 diabetic patients.
Identification of autoantibody-negative autoimmune type 2 diabetic patients.
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DOI:
10.2337/dc10-0579
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发表时间:
2011-01
期刊:
影响因子:
16.2
通讯作者:
Palmer JP
中科院分区:
文献类型:
--
作者:
Brooks-Worrell BM;Reichow JL;Goel A;Ismail H;Palmer JP
Islet autoimmunity has long been recognized in the pathogenesis of type 1 diabetes and is becoming increasingly acknowledged as a component in the pathogenesis of type 2 diabetes. Islet reactive T cells and autoantibodies have been demonstrated in type 1 diabetes, whereas islet autoimmunity in type 2 diabetes has been limited to islet autoantibodies. In this study, we investigated whether islet reactive T cells might also be present in type 2 diabetic patients and how islet reactive T cells correlate with β-cell function. Adult phenotypic type 2 diabetic patients (n = 36) were screened for islet reactive T-cell responses using cellular immunoblotting and five islet autoantibodies (islet cell antibody, GADA, insulin autoantibody, insulinoma-associated protein-2 autoantibody, and zinc transporter autoantibody). We identified four subgroups of adult phenotypic type 2 diabetic patients based on their immunological status (Ab−T−, Ab+T−, Ab−T+, and Ab+T+). The Ab−T+ type 2 diabetic patients demonstrated T-cell responses similar to those of the Ab+T+ type 2 diabetic patients. Data were adjusted for BMI, insulin resistance, and duration of diabetes. Significant differences (P < 0.02) were observed among groups for fasting and glucagon-stimulated C-peptide responses. T-cell responses to islet proteins were also demonstrated to fluctuate less than autoantibody responses. We have identified a group of adult autoimmune phenotypic type 2 diabetic patients who are Ab−T+ and thus would not be detected using autoantibody testing alone. We conclude that islet autoimmunity may be more prevalent in adult phenotypic type 2 diabetic patients than previously estimated.
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影响因子:
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作者:
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通讯作者:
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影响因子:
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DOI:
10.1073/pnas.0705894104
发表时间:
2007-10-23
影响因子:
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作者:
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作者:
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作者:
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通讯作者:
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