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

被引:253
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
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
收藏
页码:670 / 675
页数:6
相关论文
共 59 条
  • [1] Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4(+) TH1-like responses
    Berg, DJ
    Davidson, N
    Kuhn, R
    Muller, W
    Menon, S
    Holland, G
    ThompsonSnipes, L
    Leach, MW
    Rennick, D
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (04) : 1010 - 1020
  • [2] Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
    Bettelli, E
    Carrier, YJ
    Gao, WD
    Korn, T
    Strom, TB
    Oukka, M
    Weiner, HL
    Kuchroo, VK
    [J]. 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
    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
    [J]. 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
    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
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (05) : 1317 - 1326
  • [8] Selective regulatory function of Socs3 in the formation of IL-17-secreting T cells
    Chen, Zhi
    Laurence, Arian
    Kanno, Yuka
    Pacher-Zavisin, Margit
    Zhu, Bing-Mei
    Tato, Cristina
    Yoshimura, Akihiko
    Hennighausen, Lothar
    O'Shea, John J.
    [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
    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
    [J]. 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
    Cho, ML
    Yoon, CH
    Hwang, SY
    Park, MK
    Min, SY
    Lee, SH
    Park, SH
    Kim, HY
    [J]. ARTHRITIS AND RHEUMATISM, 2004, 50 (03): : 776 - 784