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CD 127 − and FoxP3 + Expression on CD25 + CD4 + T Regulatory Cells upon Specific Diabetogeneic Stimulation in High‐risk Relatives of Type 1 Diabetes Mellitus Patients
Author(s) -
Vrabelova Z.,
Hrotekova Z.,
Hladikova Z.,
Bohmova K.,
Stechova K.,
Michalek J.
Publication year - 2008
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2008.02074.x
Subject(s) - foxp3 , il 2 receptor , interleukin 7 receptor , type 1 diabetes , immunology , human leukocyte antigen , medicine , endocrinology , biology , regulatory t cell , diabetes mellitus , t cell , antigen , immune system
Abnormalities in CD4 + CD25 + regulatory T cells (Treg) may contribute to type 1 diabetes (T1D) development. First‐degree relatives of T1D patients are at increased risk especially when they carry certain HLA II haplotypes. Using two novel markers of CD4 + CD25 + Treg (CD127 − and FoxP3 + respectively), we evaluated number and function of Treg after specific stimulation with diabetogeneic autoantigens in 11 high‐risk (according to HLA‐linked risk) relatives of T1D patients and 14 age‐matched healthy controls using a cytokine secretion assay based on interferon‐ γ (IFN‐ γ ) production. High‐risk relatives of T1D patients had significantly lower pre‐ and post‐stimulatory number of CD127 − Treg than that of healthy controls ( P < 0.05). Labelling Treg with FoxP3 + demonstrated similar trend but did not reach statistical significance. Although the stimulation with diabetogenic autoantigens did not lead to a significant change in number of Treg in both groups, the defective function of Treg was performed by significantly higher activation of diabetogeneic T cells in high‐risk relatives of T1D patients compared to healthy controls ( P ≤ 0.02). Individuals at increased HLA‐associated genetic risk for T1D showed defects in Treg.