Role of the immune system in the maintenance of mouse facial motoneuron viability after nerve injury

被引:44
作者
Jones, KJ [1 ]
Serpe, CJ
Byram, SC
DeBoy, CA
Sanders, VM
机构
[1] Loyola Univ, Dept Cell Biol Neurobiol & Anat, Maywood, IL 60153 USA
[2] Edward Hines Jr VA Hosp, Res & Dev Serv, Hines, IL 60141 USA
[3] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA
关键词
facial motoneuron; facial nerve injury; CD4(+) T cell; neurotrophic factors; immunodeficient mouse models;
D O I
10.1016/j.bbi.2004.05.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In the field of neuroimmunology, an emerging area of research involves the role that the immune system plays in neural injury and repair. Such immune:neural interactions may involve both neuroprotective and neurodestruction actions. To begin to address the compelling, and clinically relevant, issue of how the immune system impacts neural reparative processes, we combined the well described facial nerve injury paradigm, a simple neural injury model, with various immunodeficient mouse models, in order to delineate the contributing immune cells/factors involved in neural injury and repair. We have discovered a role for the CD4(+) T cell in mediating facial motoneuron survival after facial nerve injury in the mouse. In this review, we present an overview of our work to date in this field and discuss future directions relevant to understanding key elements in the crosstalk between the immune:neural systems that develops subsequent to injury and/or trauma. (C) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:12 / 19
页数:8
相关论文
共 31 条
[1]   Regulation of T-cell responses by CNS antigen-presenting cells: different roles for microglia and astrocytes [J].
Aloisi, F ;
Ria, F ;
Adorini, L .
IMMUNOLOGY TODAY, 2000, 21 (03) :141-147
[2]  
Becher B, 2000, GLIA, V29, P293
[3]  
Benveniste EN, 1997, CHEM IMMUNOL, V69, P31
[4]   A SEVERE COMBINED IMMUNODEFICIENCY MUTATION IN THE MOUSE [J].
BOSMA, GC ;
CUSTER, RP ;
BOSMA, MJ .
NATURE, 1983, 301 (5900) :527-530
[5]   CD4-positive T cell-mediated neuroprotection requires dual compartment antigen presentation [J].
Byram, SC ;
Carson, MJ ;
DeBoy, CA ;
Serpe, CJ ;
Sanders, VM ;
Jones, KJ .
JOURNAL OF NEUROSCIENCE, 2004, 24 (18) :4333-4339
[6]   Natural killer cells do not mediate facial motoneuron survival after facial nerve transection [J].
Byram, SC ;
Serpe, CJ ;
Pruett, SB ;
Sanders, VM ;
Jones, KJ .
BRAIN BEHAVIOR AND IMMUNITY, 2003, 17 (06) :417-425
[7]   Differential abilities of central nervous system resident endothelial cells and astrocytes to serve as inducible antigen-presenting cells [J].
Girvin, AM ;
Gordon, KB ;
Welsh, CJ ;
Clipstone, NA ;
Miller, SD .
BLOOD, 2002, 99 (10) :3692-3701
[8]   Neuroprotection by encephalomyelitis:: Rescue of mechanically injured neurons and neurotrophin production by CNS-infiltrating T and natural killer cells [J].
Hammarberg, H ;
Lidman, O ;
Lundberg, C ;
Eltayeb, SY ;
Gielen, AW ;
Muhallab, S ;
Svenningsson, A ;
Lindå, H ;
van der Meide, PH ;
Cullheim, S ;
Olsson, T ;
Piehl, F .
JOURNAL OF NEUROSCIENCE, 2000, 20 (14) :5283-5291
[9]   PERIVASCULAR MICROGLIAL CELLS OF THE CNS ARE BONE-MARROW DERIVED AND PRESENT ANTIGEN INVIVO [J].
HICKEY, WF ;
KIMURA, H .
SCIENCE, 1988, 239 (4837) :290-292
[10]  
Ide C, 1996, NEUROSCI RES, V25, P101