Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines

doi:10.1002/jnr.10621

	Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines
	Raivich, G ; Bohatschek, M ; Werner, A ; Jones, LL ; Galiano, M ; Kloss, CUA ; Zhu, XZ ; Pfeffer, K ; Liu, ZQ
刊名	JOURNAL OF NEUROSCIENCE RESEARCH
	2003-06-15
卷号	72 期号:6 页码:726-733
关键词	rodents T-lymphocytes cytokine receptors neuroimmunology cell trafficking
ISSN号	0360-4012
DOI	10.1002/jnr.10621
文献子类	Article
英文摘要	Studies using mouse axotomised facial motoneuron model show a strong and highly selective entry of CD3+ lymphocytes into the affected nucleus, with a maximum at Day 14, which coincides with the peak of neuronal cell death, microglial phagocytosis, and increased synthesis of interleukin-1 beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and interferon-gamma (IFNgamma) We explored the possible involvement of these cytokines during the main phase of lymphocyte recruitment into the axotomised facial motor nucleus 7-21 days after nerve cut using mice homozygously deficient for IL1 receptor type 1 (IL1R1(-/-)), TNF receptor type 1 (TNFR1(-/-)), type 2 (TNFR2(-/-)) and type 1 and 2 (TNFR1&2(-/-)), IFNgamma receptor type 1 (IFNgammaR1(-/-)), and the appropriate controls for the genetic background. Transgenic deletion of IL1R1 led to a 54% decrease and that of TNFR2 to a 44% reduction in the number of CD3+ T-cells in the axotomised facial motor nucleus, with a similar relative decrease at Day 7, 14, and 21. Deletion of TNFR1 or IFNgammaR1 had no significant effect. Deletion of both TNFR1 and 2 (TNFR1&2(-/-)) caused a somewhat stronger, 63% decrease than did TNFR2 deletion alone, but this could be due to an almost complete inhibition of neuronal cell death. No mutations seemed to inhibit aggregation of CD3+ T-cells around glial nodules consisting of Ca-ion binding adaptor protein-1 (IBA1)+ phagocytotic microglia and neuronal debris. Altogether, the current data show the importance of IL1R1 and TNFR2 as the key players during the main phase of lymphocyte recruitment to the damaged part of the central nervous system. (C) 2003 Wiley-Liss, Inc.
WOS关键词	FACIAL MOTOR NUCLEUS ; CENTRAL-NERVOUS-SYSTEM ; TUMOR-NECROSIS-FACTOR ; NEUROGLIAL ACTIVATION ; INFLAMMATORY RESPONSE ; DEFICIENT MICE ; SPINAL-CORD ; MICROGLIAL ACTIVATION ; IMMUNE SURVEILLANCE ; INTERFERON-GAMMA
WOS研究方向	Neurosciences & Neurology
语种	英语
出版者	WILEY-BLACKWELL
WOS记录号	WOS:000183381000008
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/274220]
专题	中国科学院上海药物研究所
通讯作者	Raivich, G
作者单位	1.UCL, Dept Anat, London WC1E 6HX, England 2.Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-8000 Munich, Germany 3.UCL, Dept Obstet & Gynaecol, Perinatal Brain Repair Grp, London WC1E 6HX, England 4.Max Planck Inst Neurobiol, Dept Neuromorphol, Martinsried, Germany 5.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China
推荐引用方式 GB/T 7714	Raivich, G,Bohatschek, M,Werner, A,et al. Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2003,72(6):726-733.
APA	Raivich, G.,Bohatschek, M.,Werner, A.,Jones, LL.,Galiano, M.,...&Liu, ZQ.(2003).Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines.JOURNAL OF NEUROSCIENCE RESEARCH,72(6),726-733.
MLA	Raivich, G,et al."Lymphocyte infiltration in the injured brain: Role of proinflammatory cytokines".JOURNAL OF NEUROSCIENCE RESEARCH 72.6(2003):726-733.