The Spatio-Temporal Expression Profiles of CD4+T Cell Differentiation and Function-Related Genes During EAE Pathogenesis

被引：11

作者：

Cai, Yingying ^{[1
]}

Shen, Hu ^{[2
]}

Qin, Chaoyan ^{[1
]}

Zhou, Jinfeng ^{[1
]}

Lai, Weiming ^{[1
]}

Pan, Juping ^{[2
]}

Du, Changsheng ^{[1
,3
]}

机构：

[1] Tongji Univ, Res Ctr Translat Med, Shanghai Key Lab Signaling & Dis Res, East Hosp,Sch Life Sci & Technol, 1239 Si Ping Rd, Shanghai 200092, Peoples R China

[2] Tongji Univ, Tongji Hosp, Tongji Univ Branch, 1239 Si Ping Rd, Shanghai 200092, Peoples R China

[3] Chinese Acad Sci, Shanghai Inst Mat Med, State key Lab Drug Res, Shanghai 201203, Peoples R China

来源：

INFLAMMATION | 2017年 / 40卷 / 01期

基金：

中国国家自然科学基金;

关键词：

cytokine; experimental autoimmune encephalomyelitis; multiple sclerosis; transcription factor; REGULATORY T-CELLS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; TGF-BETA; MULTIPLE-SCLEROSIS; TH17; CELLS; INFLAMMATION; CYTOKINE; RECEPTOR; IL-10; BRAIN;

D O I：

10.1007/s10753-016-0469-1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Multiple sclerosis is a CD4(+) T cell-mediated autoimmune disease of the central nervous system. The unbalance of the cytokines and transcription factors critical for CD4(+) T cell differentiation and function is probably the main reason that causes MS. We detected the mRNA expression changes of key cytokines and transcription factors which are critical for Th1, Th2, Th17, and Treg cell differentiation and function in different tissues during EAE pathogenesis. We fund that each gene not only has its own featured expression changes, but also has interaction with one another, which composes a network of immunity. Understanding the roles of key cytokines and transcription factors in these processes will help to understand disease pathogenesis and supply indications for disease therapy.

引用

页码：195 / 204

页数：10

共 34 条

[1]

Bettelli E, 1998, J IMMUNOL, V161, P3299

[2]

Interleukin-10 Signaling in Regulatory T Cells Is Required for Suppression of Th17 Cell-Mediated Inflammation [J].