CD28- CD8+ T cells are significantly reduced and correlate with disease duration in juveniles with type 1 diabetes

被引:11
作者
Yarde, Danielle N. [1 ]
Lorenzo-Arteaga, Kristina [1 ]
Corley, Kevin P. [2 ]
Cabrera, Monina [2 ]
Sarvetnick, Nora E. [1 ]
机构
[1] Univ Nebraska, Med Ctr, Dept Surg Transplant, Omaha, NE 68198 USA
[2] Childrens Hosp & Med Ctr, Div Endocrinol, Omaha, NE 68114 USA
关键词
Juvenile type 1 diabetes; CD28(-) CD8(+) T cells; T suppressor cells; LYMPHOCYTES; CD8(+)CD28(-); FREQUENCY; CHILDREN; EXPANSION; MELLITUS; HOMEOSTASIS; TELOMERES; APOPTOSIS; DECREASE;
D O I
10.1016/j.humimm.2014.09.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Type 1 diabetes (T1D) is a chronic disease caused by autoimmune destruction of insulin-producing pancreatic beta-cells. T1D is typically diagnosed in children, but information regarding immune cell subsets in juveniles with T1D is scarce. Therefore, we studied various lymphocytic populations found in the peripheral blood of juveniles with T1D compared to age-matched controls (ages 2-17). One population of interest is the CD28(-) CD8(+) T cell subset, which are late-differentiated cells also described as suppressors. These cells are altered in a number of disease states and have been shown to be reduced in adults with T1D. We found that the proportion of CD28(-) cells within the CD8(+) T cell population is significantly reduced in juvenile type 1 diabetics. Furthermore, this reduction is not correlated with age in T1D juveniles, although a significant negative correlation between proportion CD28(-) CD8(+) T cells and age was observed in the healthy controls. Finally, correlation analysis revealed a significant and negative correlation between the proportion of CD28(-) CD8(+) T cells and T1D disease duration. These findings show that the CD28(-) CD8(+) T cell population is perturbed following onset of disease and may prove to be a valuable marker for monitoring the progression of T1D. (C) 2014 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1069 / 1074
页数:6
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