Th1/Th2 Balance and Th17/Treg-Mediated Immunity in relation to Murine Resistance to Dextran Sulfate-Induced Colitis

被引:55
|
作者
Yang, Fangli [1 ,2 ]
Wang, Danan [1 ]
Li, Yan [1 ]
Sang, Lixuan [1 ]
Zhu, Junfeng [1 ]
Wang, Jinyan [1 ]
Wei, Bing [1 ]
Lu, Changlong [1 ]
Sun, Xun [1 ]
机构
[1] China Med Univ, Dept Immunol, Shenyang 110122, Peoples R China
[2] Shenyang Med Coll, Dept Immunol, Coll Basic Med Sci, Shenyang 110034, Peoples R China
基金
中国国家自然科学基金;
关键词
INFLAMMATORY-BOWEL-DISEASE; SODIUM-INDUCED COLITIS; TH17; CELLS; T-CELLS; EXPRESSION; IL-17; DIFFERENTIATION; PATHOGENESIS; CYTOKINES; PROFILE;
D O I
10.1155/2017/7047201
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. The role of the Th17/Treg balance in the development of experimental colitis remains poorly understood. Methods. We exploited the differential response of BALB/c mice and C57BL/6 mice towards drinking water mediated by dextran sulfate sodium (DSS) challenge. Results. DSS-resistant BALB/c mice were characterized by low levels of IFN-gamma and TNF-alpha but high levels of IL-4, IL-6, IL-10, IL-17A, IL-17F, and colon lamina propria and mesenteric lymph node (MLN) CD4(+) CD25(+) FoxP3(+) T cells when compared to C57BL/6 mice. Collectively, these data indicate the propensity of BALB/c mice towards a Th2/Th17/ Treg-polarized immunity protecting these animals against DSS challenge, whereas Th1-polarization of C57BL/6 mice confers sensitivity to DSS-induced colitis. Conclusions. The intrinsic congenital capacity of mouse strains with respect to T cell proliferation determines sensitivity to experimental colitis.
引用
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页数:11
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