Th17 cells in autoimmune disease: changing the verdict

被引:15
作者
Haak, S. [1 ]
Gyuelveszi, G. [1 ]
Becher, B. [1 ]
机构
[1] Univ Zurich Hosp, Dept Pathol, Inst Expt Immunol, CH-8091 Zurich, Switzerland
关键词
autoimmunity; CNS; experimental autoimmune encephalitomyelitis; IL-17; multiple sclerosis; Th cells; CENTRAL-NERVOUS-SYSTEM; ROR-GAMMA-T; DIFFERENTIAL REGULATION; IL-17; INFLAMMATION; INDUCTION; CYTOKINE; DRIVE; MICE;
D O I
10.2217/1750743X.1.2.199
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Th17 cells and their proinflammatory signature cytokine, IL-17, have recently replaced Th1 cells to be the essential Th effector population in autoimmune disease. This was based on a similar line of evidence that previously destined Th1 cells to be the sole encephalitogenic Th-cell effector type. However, as for the Th1-effector type before, an increasing amount of evidence is accumulating that questions the pivotal role of Th17 cells in autoimmunity. Recently, four high-impact articles were published that clearly show that Th1 and Th17 cells carry encephalitogenic properties, and dominance of either in an autoimmune setting can confer disease. In two mouse models for autoimmune neuroinflammation, it was suggested that Th1 and Th17 cells act in parallel, both exhibiting a different set of effector mechanisms.
引用
收藏
页码:199 / 203
页数:5
相关论文
共 31 条
[1]   Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12 [J].
Becher, B ;
Durell, BG ;
Noelle, RJ .
JOURNAL OF CLINICAL INVESTIGATION, 2002, 110 (04) :493-497
[2]   What is the blood-brain barrier (not)? [J].
Bechmann, Ingo ;
Galea, Ian ;
Perry, V. Hugh .
TRENDS IN IMMUNOLOGY, 2007, 28 (01) :5-11
[3]   Th17: the third member of the effector T cell trilogy [J].
Bettelli, Estelle ;
Korn, Thomas ;
Kuchroo, Vijay K. .
CURRENT OPINION IN IMMUNOLOGY, 2007, 19 (06) :652-657
[4]   The Th17-ELR+ CXC chemokine pathway is essential for the development of central nervous system autoimmune disease [J].
Carlson, Thaddeus ;
Kroenke, Mark ;
Rao, Praveen ;
Lane, Thomas E. ;
Segal, Benjamin .
JOURNAL OF EXPERIMENTAL MEDICINE, 2008, 205 (04) :811-823
[5]   Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis [J].
Chen, Y ;
Langrish, CL ;
Mckenzie, B ;
Joyce-Shaikh, B ;
Stumhofer, JS ;
McClanahan, T ;
Blumenschein, W ;
Churakovsa, T ;
Low, J ;
Presta, L ;
Hunter, CA ;
Kastelein, RA ;
Cua, DJ .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (05) :1317-1326
[6]   Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain [J].
Cua, DJ ;
Sherlock, J ;
Chen, Y ;
Murphy, CA ;
Joyce, B ;
Seymour, B ;
Lucian, L ;
To, W ;
Kwan, S ;
Churakova, T ;
Zurawski, S ;
Wiekowski, M ;
Lira, SA ;
Gorman, D ;
Kastelein, RA ;
Sedgwick, JD .
NATURE, 2003, 421 (6924) :744-748
[7]   An essential function for the nuclear receptor RORγt in the generation of fetal lymphoid tissue inducer cells [J].
Eberl, G ;
Marmon, S ;
Sunshine, MJ ;
Rennert, PD ;
Choi, YW ;
Littman, DR .
NATURE IMMUNOLOGY, 2004, 5 (01) :64-73
[8]  
Eugster HP, 1998, EUR J IMMUNOL, V28, P2178, DOI 10.1002/(SICI)1521-4141(199807)28:07<2178::AID-IMMU2178>3.0.CO
[9]  
2-D
[10]  
Ferber IA, 1996, J IMMUNOL, V156, P5