IL-12Rβ2 has a protective role in relapsing-remitting experimental autoimmune encephalomyelitis

被引：9
|
作者：
Xie, Chong [1 ,2 ]
Ciric, Bogoljub [1 ]
Yu, Shuo [1 ]
Zhang, Guang-Xian [1 ]
Rostami, Abdolmohamad [1 ]
机构：
[1] Thomas Jefferson Univ, Dept Neurol, 901 Walnut St,Suite 400, Philadelphia, PA 19107 USA
[2] Second Mil Med Univ, Changhai Hosp, Dept Neurol, Shanghai 200433, Peoples R China
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2016年 / 291卷
关键词：
Experimental autoimmune encephalomyelitis (EAE); IL-12R beta 2; Relapse; IL-12; IL-35; CENTRAL-NERVOUS-SYSTEM; CD4(+)CD25(-)FOXP3(+) T-CELLS; IL-12 RECEPTOR BETA-2; CYTOKINE GM-CSF; ROR-GAMMA-T; IFN-GAMMA; INTERFERON-GAMMA; MULTIPLE-SCLEROSIS; IMMUNOREGULATORY FUNCTIONS; HETERODIMERIC CYTOKINE;
D O I：
10.1016/j.jneuroim.2015.12.009
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
IL-12R beta 2 is a common receptor subunit of heterodimeric receptors for IL-12 and IL-35, two cytokines that are implicated in immunopathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. We evaluated the role of IL-12R beta 2 in relapsing-remitting EAE (RR-EAE). IL-12R beta 2-deficient SJL/J mice developed markedly more severe clinical EAE, and had greater mortality and more severe relapses compared with wild-type controls. IL-12R beta 2-deficient EAE mice also had more infiltrating mononuclear cells in the CNS, as well as higher T cell proliferative capacity and decreased IFN-gamma production at the periphery. These findings demonstrate a protective role of IL-12R beta 2 in RR-EAE. (C) 2015 Published by Elsevier B.V.
引用
收藏
页码：59 / 69
页数：11
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