TH-17:: a giant step from TH1 and TH2

被引：124

作者：

Wynn, TA ^{[1
]}

机构：

[1] NIAID, NIH, Bethesda, MD 20892 USA

来源：

NATURE IMMUNOLOGY | 2005年 / 6卷 / 11期

关键词：

D O I：

10.1038/ni1105-1069

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

CD4+ T cells have been classically separated into two dominant effector populations: T helper types 1 and 2. Two new studies suggest that T cells producing interleukin 17 constitute a previously unknown lineage of CD4+ T cells.

引用

页码：1069 / 1070

页数：3

共 12 条

[1] 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

[2] 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

[3] Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages [J].

Harrington, LE ;

Hatton, RD ;

Mangan, PR ;

Turner, H ;

Murphy, TL ;

Murphy, KM ;

Weaver, CT .

NATURE IMMUNOLOGY, 2005, 6 (11) :1123-1132

[4] Interleukin-17 family members and inflammation [J].

Kolls, JK ;

Lindén, A .

IMMUNITY, 2004, 21 (04) :467-476

[5] IL-23 drives a pathogenic T cell population that induces autoimmune inflammation [J].

Langrish, CL ;

Chen, Y ;

Blumenschein, WM ;

Mattson, J ;

Basham, B ;

Sedgwick, JD ;

McClanahan, T ;

Kastelein, RA ;

Cua, DJ .

JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 201 (02) :233-240

[6] Divergent pro- and Antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation [J].

Murphy, CA ;

Langrish, CL ;

Chen, Y ;

Blumenschein, C ;

McClanahan, T ;

Kastelein, RA ;

Sedgwick, JD ;

Cua, DJ .

JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (12) :1951-1957

[7] Antigen-specific T cell Sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses [J].

Nakae, S ;

Komiyama, Y ;

Nambu, A ;

Sudo, K ;

Iwase, M ;

Homma, I ;

Sekikawa, K ;

Asano, M ;

Iwakura, Y .

IMMUNITY, 2002, 17 (03) :375-387

[8] IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist [J].

Nakae, S ;

Saijo, S ;

Horai, R ;

Sudo, K ;

Mori, S ;

Iwakura, Y .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (10) :5986-5990

[9] Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12 [J].

Oppmann, B ;

Lesley, R ;

Blom, B ;

Timans, JC ;

Xu, YM ;

Hunte, B ;

Vega, F ;

Yu, N ;

Wang, J ;

Singh, K ;

Zonin, F ;

Vaisberg, E ;

Churakova, T ;

Liu, MR ;

Gorman, D ;

Wagner, J ;

Zurawski, S ;

Liu, YJ ;

Abrams, JS ;

Moore, KW ;

Rennick, D ;

de Waal-Malefyt, R ;

Hannum, C ;

Bazan, JF ;

Kastelein, RA .

IMMUNITY, 2000, 13 (05) :715-725

[10] A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rβ1 and a novel cytokine receptor subunit, IL-23R [J].

Parham, C ;

Chirica, M ;

Timans, J ;

Vaisberg, E ;

Travis, M ;

Cheung, J ;

Pflanz, S ;

Zhang, R ;

Singh, KP ;

Vega, F ;

To, W ;

Wagner, J ;

O'Farrell, AM ;

McClanahan, T ;

Zurawski, S ;

Hannum, C ;

Gorman, D ;

Rennick, DM ;

Kastelein, RA ;

Malefyt, RD ;

Moore, KW .

JOURNAL OF IMMUNOLOGY, 2002, 168 (11) :5699-5708

← 1 2 →