Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8842204 | Progress in Neurobiology | 2017 | 74 Pages |
Abstract
Perinatal hypoxia-ischemia remains the primary cause of acute neonatal brain injury, leading to a high mortality rate and long-term neurological deficits, such as behavioral, social, attentional, cognitive and functional motor deficits. An ever-increasing body of evidence shows that the immune response to acute cerebral hypoxia-ischemia is a major contributor to the pathophysiology of neonatal brain injury. Hypoxia-ischemia provokes an intravascular inflammatory cascade that is further augmented by the activation of resident immune cells and the cerebral infiltration of peripheral immune cells response to cellular damages in the brain parenchyma. This prolonged and/or inappropriate neuroinflammation leads to secondary brain tissue injury. Yet, the long-term effects of immune activation, especially the adaptive immune response, on the hypoxic-ischemic brain still remain unclear. The focus of this review is to summarize recent advances in the understanding of post-hypoxic-ischemic neuroinflammation triggered by the innate and adaptive immune responses and to discuss how these mechanisms modulate the brain vulnerability to injury. A greater understanding of the reciprocal interactions between the hypoxic-ischemic brain and the immune system will open new avenues for potential immunomodulatory therapy in the treatment of neonatal brain injury.
Keywords
PD-L1ICAM-1TCrEAEDCsTLRHMGB1APCsPNDMHC-IISOCS1miRNAsHIETNF-R1High-mobility group protein B1DAMPsMmpsRHIL-1raSTAT3ROSAdenosine TriphosphateATPNeonatal brain injuryAntigen presenting cellsexperimental autoimmune encephalomyelitisHypoxic-ischemic encephalopathyNeuroinflammationToll-like receptorCord bloodImmunomodulatory therapyCNSpostnatal daymicroRNAsblood brain barrierBBBDendritic cellscentral nervous systemgranulocyte colony-stimulating factorG-CSFPeriventricular leukomalaciaCSFCerebrospinal fluidsignal transducer and activator of transcription 3Matrix metalloproteinasesprogrammed death-ligand 1bone marrowPVLIntercellular adhesion molecule 1knock-outNitric oxideTherapeutic hypothermiahypoxic-ischemicInflammatory mediatorsInnate immune responseAdaptive immune responseSHIP-1Reactive oxygen speciesT cell receptor
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Authors
Bo Li, Katherine Concepcion, Xianmei Meng, Lubo Zhang,