The IL-23/Th17axis:: therapeutic targets for autoimmune inflammation

被引：254

作者：

Kikly, Kristine ^{[1
]}

Liu, Ling ^{[1
]}

Na, Songqing ^{[1
]}

Sedgwick, Jonathon D. ^{[1
]}

机构：

[1] Eli Lilly & Co, Indianapolis, IN 46285 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 2006年 / 18卷 / 06期

关键词：

D O I：

10.1016/j.coi.2006.09.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Autoimmune inflammatory responses and the diseases that develop as a consequence are now thought to be driven through a novel non-Th-1 pathway. IL-23, together with additional factors including TGF-beta 1 and IL-6, collectively generate and sustain a distinct CD4(+) 'Th-17 inflammation effector' T-cell subset characterized by its production of inflammatory chemokines and cytokines, including IL-17. With this paradigm shift in understanding of autoimmune inflammation pathogenesis comes exciting opportunities to identify and to target therapeutically molecules within the IL-23/Th-17 axis that are key to disease development.

引用

页码：670 / 675

页数：6

共 59 条

[1] Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses [J].

Berg, DJ ;

Davidson, N ;

Kuhn, R ;

Muller, W ;

Menon, S ;

Holland, G ;

ThompsonSnipes, L ;

Leach, MW ;

Rennick, D .

JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (04) :1010-1020

[2] 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

[3]

Campbell IK, 1998, J IMMUNOL, V161, P3639

[4]

Chabaud M, 1999, ARTHRITIS RHEUM-US, V42, P963, DOI 10.1002/1529-0131(199905)42:5<963::AID-ANR15>3.0.CO

[5]

2-E

[6] Alefacept reduces infiltrating T cells, activated dendritic cells, and inflammatory genes in psoriasis vulgaris [J].

Chamian, F ;

Lowes, MA ;

Lin, SL ;

Lee, E ;

Kikuchi, T ;

Gilleaudeau, P ;

Sullivan-Whalen, M ;

Cardinale, I ;

Khatcherian, A ;

Novitskaya, I ;

Wittkowski, KM ;

Krueger, JG .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (06) :2075-2080

[7] 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

[8] Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells [J].

Chen, Zhi ;

Laurence, Arian ;

Kanno, Yuka ;

Pacher-Zavisin, Margit ;

Zhu, Bing-Mei ;

Tato, Cristina ;

Yoshimura, Akihiko ;

Hennighausen, Lothar ;

O'Shea, John J. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (21) :8137-8142

[9] STAT3 and NF-κB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice [J].

Cho, Mi-La ;

Kang, Jung-Won ;

Moon, Young-Mee ;

Nam, Hyo-Jung ;

Jhun, Joo-Yeon ;

Heo, Seong-Beom ;

Jin, Hyun-Tak ;

Min, So-Youn ;

Ju, Ji-Hyeon ;

Park, Kyung-Su ;

Cho, Young-Gyu ;

Yoon, Chong-Hyeon ;

Park, Sung-Hwan ;

Sung, Young-Chul ;

Kim, Ho-Youn .

JOURNAL OF IMMUNOLOGY, 2006, 176 (09) :5652-5661

[10] Effector function of type II collagen-stimulated T cells from rheumatoid arthritis patients - Cross-talk between T cells and synovial fibroblasts [J].

Cho, ML ;

Yoon, CH ;

Hwang, SY ;

Park, MK ;

Min, SY ;

Lee, SH ;

Park, SH ;

Kim, HY .

ARTHRITIS AND RHEUMATISM, 2004, 50 (03) :776-784

← 1 2 3 4 5 6 →