CXCL12 in control of neuroinflammation

被引:29
作者
Momcilovic, Miljana [1 ]
Mostarica-Stojkovic, Marija [2 ]
Miljkovic, Djordje [1 ]
机构
[1] Univ Belgrade, Inst Biol Res Sinisa Stankovic, Dept Immunol, Belgrade 11000, Serbia
[2] Univ Belgrade, Inst Microbiol & Immunol, Sch Med, Belgrade, Serbia
关键词
Experimental autoimmune encephalomyelitis; Multiple sclerosis; Neuroinflammation; CXCL12; Nitric oxide; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CELL-DERIVED FACTOR; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; CHEMOKINE RECEPTOR CXCR4; MESENCHYMAL STEM-CELLS; NITRIC-OXIDE SYNTHASE; BLOOD-BRAIN-BARRIER; DARK AGOUTI RATS; MULTIPLE-SCLEROSIS;
D O I
10.1007/s12026-012-8282-x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammation within the central nervous system (CNS) is strictly controlled and if possible prevented. Such a tight control is necessary due to high sensitivity of nervous tissue to mechanical and biochemical consequences of inflammation. Still, neuroinflammation is a typical feature of a chronic, inflammatory, demyelinating disease multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). It is assumed that mechanisms that should prevent activation of immune cells at the periphery, in the lymphoid tissues, and/or inflammation within the CNS are inadequately efficient in MS patients. Here, some recent data about the importance of CXCL12 for regulation of neuroinflammation and contribution of its deviant expression within the CNS to EAE and MS pathogenesis are presented.
引用
收藏
页码:53 / 63
页数:11
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