Interleukin-18 is a unique cytokine that stimulates both Th1 and Th2 responses depending on its cytokine milieu

被引:601
作者
Nakanishi, K
Yoshimoto, T
Tsutsui, H
Okamura, H
机构
[1] Hyogo Coll Med, Dept Immunol & Med Zool, Nishinomiya, Hyogo 6638501, Japan
[2] Hyogo Coll Med, Inst Adv Med Sci, Host Def Lab, Nishinomiya, Hyogo 6638501, Japan
[3] Japan Sci & Technol Corp, Core Res Evolut Sci Technol, Tokyo, Japan
关键词
interleukin-18; inflammatory immune responses; atopic immune responses; host defense; pathogenesis;
D O I
10.1016/S1359-6101(00)00015-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
IL-18 is a potent proinflammatory cytokine able to induce IFN gamma, GM-CSF, TNF alpha and IL-1 in immunocompetent cells, to activate killing by lymphocytes, and to up-regulate the expression of certain chemokine receptors. IL-18 is also essential to host defences against severe infections. In particular, the clearance of intracellular bacteria, fungi and protozoa requires the induction of host-derived IFN gamma, which evokes effector molecules such as nitric oxide. Also, IL-18 plays a part in the clearance of viruses, partly by the induction of cytotoxic T cells, and the expulsion of viruses is impaired in IL-18-deficient mice. IL-18 also enhances tumour rejection by its potent capacity to augment the cytotoxic activity of NK and T cells in vivo. In contrast, recent studies also demonstrate a convincing role for IL-18 in atopic responses, including atopic asthma. IL-18 induces naive T cells to develop into Th2 cells. Moreover, IL-18 also induces IL-13 and/or IL-4 production by NK cells, mast cells and basophils. Therefore, IL-18 should be seen as a unique cytokine that enhances innate immunity and both Th1- and Th2-driven immune responses. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:53 / 72
页数:20
相关论文
共 234 条
[1]   Identification of HLA-class-II-restricted epitopes of autoantigens in transgenic mice [J].
Abraham, RS ;
David, CS .
CURRENT OPINION IN IMMUNOLOGY, 2000, 12 (01) :122-129
[2]   Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function [J].
Adachi, O ;
Kawai, T ;
Takeda, K ;
Matsumoto, M ;
Tsutsui, H ;
Sakagami, M ;
Nakanishi, K ;
Akira, S .
IMMUNITY, 1998, 9 (01) :143-150
[3]  
Ahn HJ, 1997, J IMMUNOL, V159, P2125
[4]   Cloning and expression of interleukin-18 binding protein [J].
Aizawa, Y ;
Akita, K ;
Taniai, M ;
Torigoe, K ;
Mori, T ;
Nishida, Y ;
Ushio, S ;
Nukada, Y ;
Tanimoto, T ;
Ikegami, H ;
Ikeda, M ;
Kurimoto, M .
FEBS LETTERS, 1999, 445 (2-3) :338-342
[5]   The role of IL-18 in innate immunity [J].
Akira, S .
CURRENT OPINION IN IMMUNOLOGY, 2000, 12 (01) :59-63
[6]  
André-Schmutz I, 1999, EUR J IMMUNOL, V29, P245, DOI 10.1002/(SICI)1521-4141(199901)29:01<245::AID-IMMU245>3.3.CO
[7]  
2-F
[8]  
BAEUERLE PA, 1994, ANNU REV IMMUNOL, V12, P141, DOI 10.1146/annurev.immunol.12.1.141
[9]   CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1α and IP-10 are expressed in demyelinating brain lesions [J].
Balashov, KE ;
Rottman, JB ;
Weiner, HL ;
Hancock, WW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (12) :6873-6878
[10]  
Barbulescu K, 1998, J IMMUNOL, V160, P3642