Vrabelova Z, Hrotekova Z, Hladikova Z, Bohmova K, Stechova K, Michalek J
Department of Pediatrics, University Hospital Motol, Prague, Czech Republic.
Scand J Immunol. 2008 Apr;67(4):404-10. doi: 10.1111/j.1365-3083.2008.02074.x. Epub 2008 Feb 1.
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-gamma (IFN-gamma) 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 < or = 0.02). Individuals at increased HLA-associated genetic risk for T1D showed defects in Treg.
CD4+CD25+调节性T细胞(Treg)异常可能促使1型糖尿病(T1D)的发生。T1D患者的一级亲属患病风险增加,尤其是当他们携带某些HLA II单倍型时。我们使用两种新型的CD4+CD25+ Treg标志物(分别为CD127-和FoxP3+),通过基于干扰素-γ(IFN-γ)产生的细胞因子分泌试验,评估了11名(根据HLA相关风险)T1D患者的高危亲属和14名年龄匹配的健康对照在受到致糖尿病自身抗原特异性刺激后Treg的数量和功能。T1D患者的高危亲属在刺激前后CD127- Treg的数量显著低于健康对照(P < 0.05)。用FoxP3+标记Treg显示出类似趋势,但未达到统计学显著性。虽然致糖尿病自身抗原刺激在两组中均未导致Treg数量的显著变化,但与健康对照相比,T1D患者高危亲属中致糖尿病T细胞的显著更高激活表现出Treg的功能缺陷(P ≤ 0.02)。HLA相关遗传风险增加的T1D个体表现出Treg缺陷。