IL-18:: a key player in neuroinflammation and neurodegeneration?

被引:188
作者
Felderhoff-Mueser, U
Schmidt, OI
Oberholzer, A
Bührer, C
Stahel, PF
机构
[1] Charite Univ Berlin, Sch Med, Dept Trauma & Reconstruct Surg, D-12200 Berlin, Germany
[2] Charite Univ Berlin, Sch Med, Dept Neonatol, D-13353 Berlin, Germany
[3] Univ Basel, Childrens Hosp, CH-4005 Basel, Switzerland
关键词
D O I
10.1016/j.tins.2005.06.008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Interleukin (IL)-18 is a potent inflammatory cytokine of the IL-1 family. It is synthesized as an inactive precursor (pro-IL-18), which is cleaved into its functionally active form by caspase-1. Resident cells of the CNS express IL-18 and caspase-1 constitutively, thus providing a local IL-18-dependent immune response. Recent studies have highlighted a crucial role for IL-18 in mediating neuroinflammation and neurodegeneration in the CNS under pathological conditions, such as bacterial and viral infection, autoimmune demyelinating disease, and hypoxic-ischemic, hyperoxic and traumatic brain injuries. This review provides a synopsis of the current knowledge of IL-18-dependent mechanisms of action during acute neurodegeneration in immature and adult brains.
引用
收藏
页码:487 / 493
页数:7
相关论文
共 68 条
[1]   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
[2]   Inflammation in central nervous system injury [J].
Allan, SM ;
Rothwell, NJ .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 2003, 358 (1438) :1669-1677
[3]   Cytokines and acute neurodegeneration [J].
Allan, SM ;
Rothwell, NJ .
NATURE REVIEWS NEUROSCIENCE, 2001, 2 (10) :734-744
[4]   Spin precession observation in quantum corrections to resistance of Si0.7Ge0.3/Si0.2Ge0.8 heterostructure with 2DHG [J].
Andrievskii, VV ;
Komnik, YF ;
Myronov, M ;
Mironov, OA ;
Rozheshchenko, A ;
Whall, TE .
PHYSICA E-LOW-DIMENSIONAL SYSTEMS & NANOSTRUCTURES, 2003, 18 (1-3) :145-146
[5]  
[Anonymous], CURR OPIN CRIT CARE
[6]   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
[7]   IL-23 produced by CNS-resident cells controls T cell encephalitogenicity during the effector phase of experimental autoimmune encephalomyelitis [J].
Becher, B ;
Durell, BG ;
Noelle, RJ .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (08) :1186-1191
[8]   Cytokine-mediated inflammation, tumorigenesis, and disease-associated JAK/STAT/SOCS signaling circuits in the CNS [J].
Campbell, IL .
BRAIN RESEARCH REVIEWS, 2005, 48 (02) :166-177
[9]   Multiple sclerosis: Cytokine receptors on oligodendrocytes predict innate regulation [J].
Cannella, B ;
Raine, CS .
ANNALS OF NEUROLOGY, 2004, 55 (01) :46-57
[10]   Activation of intrinsic and extrinsic proapoptotic signaling pathways in interleukin-18-mediated human cardiac endothelial cell death [J].
Chandrasekar, B ;
Vemula, K ;
Surabhi, RM ;
Li-Weber, M ;
Owen-Schaub, LB ;
Jensen, LE ;
Mummidi, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (19) :20221-20233