The inflammatory Th 17 subset in immunity against self and non-self antigens

被引:43
作者
Jin, Di [1 ,3 ]
Zhang, Lianjun [1 ,3 ]
Zheng, Jialin [2 ,3 ]
Zhao, Yong [1 ,3 ]
机构
[1] Chinese Acad Sci, Inst Zool, Transplantat Biol Res Div, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100101, Peoples R China
[2] Univ Nebraska Med Ctr, Dept Pharmacol & Expt Neurosci, Lab Neurotoxicol, Omaha, NE USA
[3] China US foint Res Ctr Med Sci & Genet, Beijing, Peoples R China
关键词
CD4(+) T cells; Th17; cells; regulatory T cells; immune regulation;
D O I
10.1080/08916930701776605
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T helper cells (Th cells) are traditionally thought to differentiate into Th1 and Th2 subsets based on their cytokine profiles. Recently, a subset of interleukin (IL)-17-producing cells (Th17 cells) which develop and function in a distinct way from Th1 or Th2 cells has been identified. Th17 cells have been shown to play a crucial role in the induction of autoimmune tissue injuries, inflammation and infection. Studies on Th17 subset and its relevant issues offered potential therapeutic targets for patients with autoimmune diseases, cancer, infection and transplant, which may have significant impacts in the prevention and/or treatment of immunity-related diseases in clinics.
引用
收藏
页码:154 / 162
页数:9
相关论文
共 95 条
[1]  
Aarvak T, 1999, J IMMUNOL, V162, P1246
[2]   Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].
Aggarwal, S ;
Ghilardi, N ;
Xie, MH ;
de Sauvage, FJ ;
Gurney, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1910-1914
[3]   ERK1-/- mice exhibit Th1 cell polarization and increased susceptibility to experimental autoimmune encephalomyelitis [J].
Agrawal, Anshu ;
Dillon, Stephanie ;
Denning, Timothy L. ;
Pulendran, Bali .
JOURNAL OF IMMUNOLOGY, 2006, 176 (10) :5788-5796
[4]   Interleukin-17 is produced by both Th1 and Th2 lymphocytes, and modulates interferon-γ- and interleukin-4-induced activation of human keratinocytes [J].
Albanesi, C ;
Scarponi, CS ;
Cavani, A ;
Federici, M ;
Nasorri, F ;
Girolomoni, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2000, 115 (01) :81-87
[5]  
Albanesi C, 1999, J IMMUNOL, V162, P494
[6]   Phenotypic and functional features of human Th17 cells [J].
Annunziato, Francesco ;
Cosmi, Lorenzo ;
Santarlasci, Veronica ;
Maggi, Laura ;
Liotta, Francesco ;
Mazzinghi, Benedetta ;
Parente, Eliana ;
Fili, Lucia ;
Ferri, Simona ;
Frosali, Francesca ;
Giudici, Francesco ;
Romagnani, Paola ;
Parronchi, Paola ;
Tonelli, Francesco ;
Maggi, Enrico ;
Romagnani, Sergio .
JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (08) :1849-1861
[7]   Interleukin 27 limits autoimmune encephalomyelitis by suppressing the development of interleukin 17-producing T cells [J].
Batten, Marcel ;
Li, Ji ;
Yi, Sothy ;
Kljavin, Noelyn M. ;
Danilenko, Dimitry M. ;
Lucas, Sophie ;
Lee, James ;
de Sauvage, Frederic J. ;
Ghilardi, Nico .
NATURE IMMUNOLOGY, 2006, 7 (09) :929-936
[8]   Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis [J].
Bettelli, E ;
Sullivan, B ;
Szabo, SJ ;
Sobel, RA ;
Glimcher, H ;
Kuchroo, VK .
JOURNAL OF EXPERIMENTAL MEDICINE, 2004, 200 (01) :79-87
[9]   Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].
Bettelli, E ;
Carrier, YJ ;
Gao, WD ;
Korn, T ;
Strom, TB ;
Oukka, M ;
Weiner, HL ;
Kuchroo, VK .
NATURE, 2006, 441 (7090) :235-238
[10]   IL-17 mRNA in sputum of asthmatic patients: linking T cell driven inflammation and granulocytic influx? [J].
Bullens, Dominique M. A. ;
Truyen, Els ;
Coteur, Liesbeth ;
Dilissen, Ellen ;
Hellings, Peter W. ;
Dupont, Lieven J. ;
Ceuppens, Jan L. .
RESPIRATORY RESEARCH, 2006, 7 (1)