Cutting Edge: The Idd3 Genetic Interval Determines Regulatory T Cell Function through CD11b+CD11c- APC

被引：17

作者：

Anderson, Ana C. ^{[1
]}

Chandwaskar, Rucha

Lee, David H.

Kuchroo, Vijay K. ^{[1
]}

机构：

[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis,Harvard Inst Med, Boston, MA 02115 USA

来源：

JOURNAL OF IMMUNOLOGY | 2008年 / 181卷 / 11期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.4049/jimmunol.181.11.7449

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

The Idd3 genetic interval confers protection against multiple autoimmune diseases, including type I diabetes and experimental autoimmune encephalomyelitis. The favored candidate gene in this interval is Il2, which is polymorphic between susceptible and resistant strains of mice. IL-2 regulates the growth/death of effector T cells as well as the generation/maintenance of regulatory T cells (Tregs), and recent studies have shown that NOD.Idd3 Tregs are more suppressive than their NOD counterparts. We have further dissected the mechanisms underlying the differential suppression by NOD and NOD.Idd3 Tregs and find that it is determined by CD11b(+)CD11c(-) APCs. Thus, contrary to what might be expected, our data suggest that the differential suppressive activity of NOD and NOD.Idd3 Tregs is not due to an effect of the Idd3 genetic interval on T cells but rather is due to differences in the APC compartment. The Journal of Immunology, 2008, 181: 7449-7452.

引用

页码：7449 / 7452

页数：4

共 22 条

[1]

Deficiency in NOD antigen-presenting cell function may be responsible for suboptimal CD4+ CD25+ T-cell-mediated regulation and type 1 diabetes development in NOD mice [J].