title: Interactions between the cells of the immune and nervous system: neurotrophins as neuroprotection mediators in CNS injury.
abstract: Inflammatory processes in the central nervous system (CNS) are considered neurotoxic, although recent studies suggest that they also can be beneficial and confer neuroprotection (neuroprotective autoimmunity). Cells from the immune system have been detected in CNS injury and found to produce and secrete a variety of neurotrophins such as NGF, BDNF, NT-3 and NT-4/5, and to express (similarly to neuronal cells), members of the tyrosine kinase (Trk) receptor family such as TrkA, TrkB and TrkC. Indeed, autocrine and paracrine interactions are observed at the site of CNS injury, resulting in a variety of homologic-heterologic modulations of immune and neuronal cell function. The end result of the inflammatory process, neurotoxicity and/or neuroprotection, is a function of the fine balance between the two cellular systems, i.e., of the complex signaling relationships between anti-inflammatory neuroprotective factors (neurotrophins and other chemical mediators) and proinflammatory neurotoxic factors (TNF, free radicals, certain cytokines, etc.). Autoimmune neuroprotection is a novel therapeutic approach aimed at shifting the balance between the immune and neuronal cells towards survival pathways in a variety of CNS injuries. This review focuses on data supporting this concept and its future therapeutical implications for optic nerve injury and multiple sclerosis.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 91120, Israel.
authors.forename: Rinat
authors.initials: R
authors.lastname: Tabakman
authors.forename: Shimon
authors.initials: S
authors.lastname: Lecht
authors.forename: Stela
authors.initials: S
authors.lastname: Sephanova
authors.forename: Hadar
authors.initials: H
authors.lastname: Arien-Zakay
authors.forename: Philip
authors.initials: P
authors.lastname: Lazarovici
mesh_terms: D000818:Animals; D006801:Humans; D007107:Immune System / Q000502:physiology*; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control; D009414:Nerve Growth Factors / Q000378:metabolism / Q000627:therapeutic use*; D009420:Nervous System / Q000276:immunology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D018696:Neuroprotective Agents / Q000378:metabolism / Q000627:therapeutic use*; D020812:Receptor, trkC / Q000235:genetics / Q000378:metabolism; D020196:Trauma, Nervous System / Q000378:metabolism / Q000517:prevention & control*
chemical_list: D009414:Nerve Growth Factors; D018696:Neuroprotective Agents; D020812:Receptor, trkC