Interleukin-10 and the regulation of mitogen-activated protein kinases:: are these signalling modules targets for the anti-inflammatory action of this cytokine?

被引:56
作者
Haddad, JJ
Saadé, NE
Safieh-Garabedian, B
机构
[1] Univ Calif San Francisco, Sch Med, Dept Anesthesia & Perioperat Care, Mol Neurosci Res Div,Severinghaus Radiometer Res L, San Francisco, CA 94143 USA
[2] Amer Univ Beirut, Fac Arts & Sci, Dept Biol, Beirut 110236, Lebanon
[3] Amer Univ Beirut, Fac Med, Dept Human Morphol & Physiol, Div Mol & Behav Neurosci, Beirut 110236, Lebanon
[4] Univ Calif San Francisco, Sch Med, San Francisco, CA 94143 USA
基金
英国医学研究理事会; 英国惠康基金; 美国国家卫生研究院;
关键词
cell signalling; cytokine; disease; IL-10; immunopharmacology; inflammation; kinase; MAPK;
D O I
10.1016/S0898-6568(02)00075-X
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The many specific, yet overlapping and redundant activities of individual cytokines have been the basis for current concepts of therapeutical intervention. Cytokines are powerful two-edged weapons that can trigger a cascade of reactions and may show activities that often go beyond the single highly specific property that it is hoped they possess. Nevertheless, it can be stated that our new, though burgeoning, understanding of the biological mechanisms governing cytokine actions is an important contribution to medical knowledge. The crucial role of the anti-inflammatory cytokine, interleukin (IL)-10, in regulating potential molecular pathway mediating injury and cell death has attracted paramount attention in recent years. In this respect, the mitogen-activated protein kinase (MAPK) components have emerged as potential signalling cascades that regulate a plethora of cell functions, including inflammation and cell death. The biochemistry and molecular biology of cytokine actions, particularly IL-10, explain some well known and sometimes also some of the more obscure clinical aspects of the evolution of diseases. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:255 / 267
页数:13
相关论文
共 145 条
[51]   The ups and downs of MEK kinase interactions [J].
Hagemann, C ;
Blank, JL .
CELLULAR SIGNALLING, 2001, 13 (12) :863-875
[52]   Signalling for survival and death in neurones - The role of stress-activated kinases, JNK and p38 [J].
Harper, SJ ;
LoGrasso, P .
CELLULAR SIGNALLING, 2001, 13 (05) :299-310
[53]   Marsupial cytokines - Structure, function and evolution [J].
Harrison, GA ;
Wedlock, DN .
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY, 2000, 24 (05) :473-484
[54]   Spermine differentially regulates the production of interleukin-12 p40 and interleukin-10 and suppresses the release of the T helper 1 cytokine interferon-γ [J].
Haskó, G ;
Kuhel, DG ;
Marton, A ;
Nemeth, ZH ;
Deitch, EA ;
Szabó, C .
SHOCK, 2000, 14 (02) :144-149
[55]   Inosine inhibits inflammatory cytokine production by a posttranscriptional mechanism and protects against endotoxin-induced shock [J].
Haskó, G ;
Kuhel, DG ;
Németh, ZH ;
Mabley, JG ;
Stachlewitz, RF ;
Virág, L ;
Lohinai, Z ;
Southan, GJ ;
Salzman, AL ;
Szabó, C .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :1013-1019
[56]   Introduction - Cytokine receptors, signaling pathways and viruses [J].
Hiscott, J .
CYTOKINE & GROWTH FACTOR REVIEWS, 2001, 12 (2-3) :129-131
[57]   Regulation of cytokine gene transcription in the immune system [J].
Holloway, AF ;
Rao, S ;
Shannon, MF .
MOLECULAR IMMUNOLOGY, 2002, 38 (08) :567-580
[58]   Nuclear factor kappa B signaling in catabolic disorders [J].
Holmes-McNary, M .
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE, 2002, 5 (03) :255-263
[59]   Anchorage-dependent ERK signaling - mechanisms and consequences [J].
Howe, AK ;
Aplin, AE ;
Juliano, RL .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2002, 12 (01) :30-35
[60]   From receptors to stress-activated MAP kinases [J].
Ichijo, H .
ONCOGENE, 1999, 18 (45) :6087-6093