Adaptive Foxp3+ regulatory T cell-dependent and -independent control of allergic inflammation

被引：339

作者：

de Lafaille, Maria A. Curotto ^{[1
,3
]}

Kutchukhidze, Nino ^{[1
]}

Shen, Shiqian ^{[1
]}

Ding, Yi ^{[1
,2
]}

Yee, Herman ^{[3
]}

Lafaille, Juan J. ^{[1
,3
]}

机构：

[1] NYU, Sch Med, Skirball Inst, Kimmel Ctr Biol & Med,Program Mol Pathogenesis, New York, NY 10016 USA

[2] NYU, Sch Med, Sackler Inst Grad Biomed Sci, New York, NY 10016 USA

[3] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA

来源：

IMMUNITY | 2008年 / 29卷 / 01期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/j.immuni.2008.05.010

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Adaptive Foxp3(+) regulatory T (Treg) cells develop during induction of mucosal tolerance and after immunization. Large numbers of Foxp3(+) T cells have been found in inflamed tissues. We investigated the role of adaptive Foxp3(+) Treg cells in mucosal tolerance and in chronic allergic lung inflammation. We used two strains of mice that are devoid of naturally occurring Treg cells; one is capable of generating adaptive Foxp3+ Treg cells upon exposure to antigen, whereas the other is deficient in both naturally occurring and adaptive Foxp3(+) Treg cells. We found that adaptive Foxp3(+) Treg cells were essential for establishing mucosal tolerance and for suppressing IL-4 production and lymphoid neogenesis in chronic inflammation, whereas IL-5 production and eosinophilia. could be controlled by Foxp3-independent IFN-gamma-dependent mechanisms. Thus, whereas adaptive Foxp3(+) Treg cells regulate sensitization to allergens and the severity of chronic inflammation, IFN-gamma-producing cells can play a beneficial role in inflammatory conditions involving eosinophils.

引用

页码：114 / 126

页数：13