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Article: Modulation of neuroimmune responses on glia in the central nervous system: Implication in therapeutic intervention against neuroinflammation

TitleModulation of neuroimmune responses on glia in the central nervous system: Implication in therapeutic intervention against neuroinflammation
Authors
Issue Date2009
Citation
Chinese Journal Of Cellular And Molecular Immunology, 2009, v. 6 n. 5, p. 317-326 How to Cite?
AbstractIt has long been known that the brain is an immunologically privileged site in normal conditions. Although the cascade of immune responses can occur as long as there is a neuronal injury or a potent immune stimulation, how the brain keeps glial cells in a quiescent state is still unclear. Increasing efforts have been made by several laboratories to elucidate how repression of immune responses is achieved in the neuronal environment. The suppression factors include neurotransmitters, neurohormones, neurotrophic factors, anti-inflammatory factors, and cell-cell contact via adhesion molecules or CD200 receptor. This review discusses how these factors affect the cascade of cerebral immune responses because no single factor listed above can fully account for the immune suppression. While several factors contribute to the suppression of immune responses, activation of glial cells and their production of pro-inflammatory factors do occur as long as there is a neuronal injury, suggesting that some neuronal components facilitate immune responses. This review also discusses which signals initiate or augment cerebral immune responses so that stimulatory signals override the suppressive signals. Increasing lines of evidence have demonstrated that immune responses in the brain are not always detrimental to neurons. Attempt to simply clear off inflammatory factors in the CNS may not be appropriate for neurons in neurological disorders. Appropriate control of immune cells in the CNS may be beneficial to neurons or even neuroregeneration. Therefore, understanding the mechanisms underlying immune suppression may help us to reshape pharmacological interventions against inflammation in many neurological disorders. © 2009 Chinese Society of Immunology and University of Science & Technology of China.
Persistent Identifierhttp://hdl.handle.net/10722/149723
ISSN
2015 SCImago Journal Rankings: 0.155
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChang, RCCen_US
dc.contributor.authorChiu, Ken_US
dc.contributor.authorHo, YSen_US
dc.contributor.authorSo, KFen_US
dc.date.accessioned2012-06-26T05:57:38Z-
dc.date.available2012-06-26T05:57:38Z-
dc.date.issued2009en_US
dc.identifier.citationChinese Journal Of Cellular And Molecular Immunology, 2009, v. 6 n. 5, p. 317-326en_US
dc.identifier.issn1007-8738en_US
dc.identifier.urihttp://hdl.handle.net/10722/149723-
dc.description.abstractIt has long been known that the brain is an immunologically privileged site in normal conditions. Although the cascade of immune responses can occur as long as there is a neuronal injury or a potent immune stimulation, how the brain keeps glial cells in a quiescent state is still unclear. Increasing efforts have been made by several laboratories to elucidate how repression of immune responses is achieved in the neuronal environment. The suppression factors include neurotransmitters, neurohormones, neurotrophic factors, anti-inflammatory factors, and cell-cell contact via adhesion molecules or CD200 receptor. This review discusses how these factors affect the cascade of cerebral immune responses because no single factor listed above can fully account for the immune suppression. While several factors contribute to the suppression of immune responses, activation of glial cells and their production of pro-inflammatory factors do occur as long as there is a neuronal injury, suggesting that some neuronal components facilitate immune responses. This review also discusses which signals initiate or augment cerebral immune responses so that stimulatory signals override the suppressive signals. Increasing lines of evidence have demonstrated that immune responses in the brain are not always detrimental to neurons. Attempt to simply clear off inflammatory factors in the CNS may not be appropriate for neurons in neurological disorders. Appropriate control of immune cells in the CNS may be beneficial to neurons or even neuroregeneration. Therefore, understanding the mechanisms underlying immune suppression may help us to reshape pharmacological interventions against inflammation in many neurological disorders. © 2009 Chinese Society of Immunology and University of Science & Technology of China.en_US
dc.languageengen_US
dc.relation.ispartofChinese Journal of Cellular and Molecular Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Diseases - Immunology - Physiopathology - Therapyen_US
dc.subject.meshCentral Nervous System - Cytology - Immunology - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmune System Processes - Immunologyen_US
dc.subject.meshImmunotherapyen_US
dc.subject.meshInflammation - Immunology - Physiopathology - Prevention & Controlen_US
dc.subject.meshNeuroglia - Immunology - Metabolismen_US
dc.subject.meshNeuroimmunomodulationen_US
dc.subject.meshSignal Transduction - Immunologyen_US
dc.titleModulation of neuroimmune responses on glia in the central nervous system: Implication in therapeutic intervention against neuroinflammationen_US
dc.typeArticleen_US
dc.identifier.emailChang, RCC:rccchang@hkucc.hku.hken_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid19887044-
dc.identifier.scopuseid_2-s2.0-70350761691en_US
dc.identifier.hkuros168107-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350761691&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume6en_US
dc.identifier.issue5en_US
dc.identifier.spage317en_US
dc.identifier.epage326en_US
dc.identifier.isiWOS:000274324100001-
dc.identifier.scopusauthoridChang, RCC=7403713410en_US
dc.identifier.scopusauthoridChiu, K=15076970500en_US
dc.identifier.scopusauthoridHo, YS=14031513600en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US

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