Limiting inflammatory responses during activation of innate immunity

被引:295
作者
Han, JH [1 ]
Ulevitch, RJ
机构
[1] Xiamen Univ, Sch Life Sci, Key Lab Minist Educ Cell Biol & Tumor Cell Engn, Xiamen 361005, Peoples R China
[2] Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA
关键词
D O I
10.1038/ni1274
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
The idea of the importance of mounting an inflammatory response for effective immunity is supported by a multiplicity of experimental data. It is also well understood that resolution of inflammation is essential for maintaining the balance between health and disease. When the normal regulatory mechanisms are disturbed, the potential for developing chronic inflammatory diseases is increased. Inflammation is a key element in the response of the innate immune system to a variety of challenges, including those provided by bacterial and viral infection as well as by damaged or dying host cells. Here we review elements of innate immunity that lead to inflammation and some of the host mechanisms that allow for the resolution of the inflammatory responses.
引用
收藏
页码:1198 / 1205
页数:8
相关论文
共 101 条
[1]
Suppressors of cytokine signalling (SOCS) in the immune system [J].
Alexander, WS .
NATURE REVIEWS IMMUNOLOGY, 2002, 2 (06) :410-416
[2]
Small-molecule inhibitors of protein-protein interactions: Progressing towards the dream [J].
Arkin, MR ;
Wells, JA .
NATURE REVIEWS DRUG DISCOVERY, 2004, 3 (04) :301-317
[3]
Interleukin-10 therapy - Review of a new approach [J].
Asadullah, K ;
Sterry, W ;
Volk, HD .
PHARMACOLOGICAL REVIEWS, 2003, 55 (02) :241-269
[4]
Suppressor of cytokine signaling (SOCS) proteins indirectly regulate toll-like receptor signaling in innate immune cells [J].
Baetz, A ;
Frey, M ;
Heeg, K ;
Dalpke, AH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (52) :54708-54715
[5]
ALTERNATIVE PROMOTER USAGE OF THE FOS-RESPONSIVE GENE FIT-1 GENERATES MESSENGER-RNA ISOFORMS CODING FOR EITHER SECRETED OR MEMBRANE-BOUND PROTEINS RELATED TO THE IL-1 RECEPTOR [J].
BERGERS, G ;
REIKERSTORFER, A ;
BRASELMANN, S ;
GRANINGER, P ;
BUSSLINGER, M .
EMBO JOURNAL, 1994, 13 (05) :1176-1188
[6]
Beutler B, 2005, ADV EXP MED BIOL, V560, P29
[7]
Oxidized phospholipids negatively regulate dendritic cell maturation induced by TLRs and CD40 [J].
Blüml, S ;
Kirchberger, S ;
Bochkov, VN ;
Krönke, G ;
Stuhlmeier, K ;
Majdic, O ;
Zlabinger, GJ ;
Knapp, W ;
Binder, BR ;
Stöckl, J ;
Leitinger, N .
JOURNAL OF IMMUNOLOGY, 2005, 175 (01) :501-508
[8]
The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses [J].
Boone, DL ;
Turer, EE ;
Lee, EG ;
Ahmad, RC ;
Wheeler, MT ;
Tsui, C ;
Hurley, P ;
Chien, M ;
Chai, S ;
Hitotsumatsu, O ;
McNally, E ;
Pickart, C ;
Ma, A .
NATURE IMMUNOLOGY, 2004, 5 (10) :1052-1060
[9]
Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors [J].
Brightbill, HD ;
Libraty, DH ;
Krutzik, SR ;
Yang, RB ;
Belisle, JT ;
Bleharski, JR ;
Maitland, M ;
Norgard, MV ;
Plevy, SE ;
Smale, ST ;
Brennan, PJ ;
Bloom, BR ;
Godowski, PJ ;
Modlin, RL .
SCIENCE, 1999, 285 (5428) :732-736
[10]
ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin tolerance [J].
Brint, EK ;
Xu, DM ;
Liu, HY ;
Dunne, A ;
McKenzie, ANJ ;
O'Neill, LAJ ;
Liew, FY .
NATURE IMMUNOLOGY, 2004, 5 (04) :373-379