Increased expression of regulatory T cell-associated markers in recent-onset diabetic children

作     者：Mikael Pihl Mikael Chéramy Jenny Mjosberg Johnny Ludvigsson Rosaura Casas 

作者机构：Division of Pediatrics and Diabetes Research CenterDepartment of Clinical and Experimental MedicineLinkoping UniversityLinkopingSweden Division of Clinical ImmunologyDepartment of Clinical and Experimental MedicineLinkoping UniversityLinkopingSweden 

出 版 物：《Open Journal of Immunology》 (免疫学期刊（英文）)

年 卷 期：2011年第1卷第3期

页      面：57-64页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：supported by the Swedish Child Diabetes Foundation the Medical Research Council of Southeast Sweden(FORSS-8847) 

主　　题：Regulatory T cells Type 1 Diabetes Autoantibodies 

摘      要：CD4+CD25hi T cells are thought to be crucial for the maintenance of immunological tolerance to self antigens. In this study, we investigated the frequencies of these cells in the early stage of type 1 diabetes, as well as in a setting of possible pre-diabetic autoimmunity. Hence, the expression of FOXP3, CTLA-4, and CD27 in CD4+ CD25hi T cells was analyzed using flow cytometry in 14 patients with recent onset type 1 diabetes, in 9 at-risk individuals, and 9 healthy individuals with no known risk for type 1 diabetes. Our results show there were no differences in the frequency of CD4+CD25hi cells between groups. However, compared to controls, recent-onset type 1 diabetic patients had higher expression of FOXP3, CTLA-4, and CD27 in CD4+ CD25hi cells from peripheral blood. The median fluorescence intensity of FOXP3 was significantly higher in CD4+CD25hi cells from patients with type 1 diabetes than from controls. Furthermore, a positive correlation between the frequency of FOXP3+ cells and the median fluorescence intensity of FOXP3 was observed among patients with type 1 diabetes. These data suggest that the frequency of CD4+CD25hi FOXP3+ T cells in the periphery is not decreased but rather increased at onset of type 1 diabetes. Thus, functional deficiencies rather than reduced numbers of CD4+CD25hi cells could contribute to the development of type 1 diabetes.