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  • [1]Yoles E, Schwartz M. Degeneration of spared axons following partial white matter lesion: implications for optic nerve neuropathies. Exp Neurol 153(1):1-7 (1998)

  • [2]Byram SC, Carson MJ, DeBoy CA. CD4-positive T cell-mediated neuroprotection requires dual compartment antigen presentation. J Neurosci 24(18):4333-9 (2004)

  • [3]Hauben E, Butovsky O, Nevo U. Passive or active immunization with myelin basic protein promotes recovery from spinal cord contusion. J Neurosci 20(17):6421-30 (2000)

  • [4]Hauben E, Nevo U, Yoles E. Autoimmune T cells as potential neuroprotective therapy for spinal cord injury. Lancet 355 (9200):286-7 (2000)

  • [5]Fitch MT, Doller C, Combs CK. Cellular and molecular mechanisms of glial scarring and progressive cavitation: in vivo and in vitro analysis of inflammation-induced secondary injury after CNS trauma. J Neurosci 19(19):8182-98 (1999)

  • [6]Ousman SS, David S. MIP-1alpha, MCP-1, GM-CSF, and TNF-alpha control the immune cell response that mediates rapid phagocytosis of myelin from the adult mouse spinal cord. J Neurosci 21(13):4649-56 (2001)

  • [7]Kipnis J, Yoles E, Porat Z. Tcell immunity to copolymer 1 confers neuroprotection on the damaged optic nerve: possible therapy for optic neuropathies. Proc Natl Acad Sci U S A 97(13):7446-51 (2000)

  • [8]Bakalash S, Kessler A, Mizrahi T. Antigenic specificity of immunoprotective therapeutic vaccination for glaucoma. Invest Ophthalmol Vis Sci 44(8):3374-81 (2003)

  • [9]Fisher J, Levkovitch-Verbin H, Schori H. Vaccination for neuroprotection in the mouse optic nerve: implications for optic neuropathies. J Neurosci 21(1):136-42 (2001)

  • [10]Hauben E, Ibarra A, Mizrahi T. Vaccination with a Nogo-A-derived peptide after incomplete spinal-cord injury promotes recovery via a T-cell-mediated neuroprotective response: comparison with other myelin antigens. Proc Natl Acad Sci U S A 98(26):15173-8 (2001)

  • [11]Schori H, Kipnis J, Yoles E. Vaccination for protection of retinal ganglion cells against death from glutamate cytotoxicity and ocular hypertension: implications for glaucoma. Proc Natl Acad Sci U S A 98(6):3398-403 (2001)

  • [12]Aloisi F. Immune function of microglia. Glia 36(2):165-79 (2001)

  • [13]Block ML, Hong JS. Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism. Prog Neurobiol 76(2):77-98 (2005)

  • [14]Ladeby R, Wirenfeldt M, Garcia-Ovejero D. Microglial cell population dynamics in the injured adult central nervous system. Brain Res Brain Res Rev 48(2):196-206 (2005)

  • [15]Sargsyan SA, Monk PN, Shaw PJ. Microglia as potential contributors to motor neuron injury in amyotrophic lateral sclerosis. Glia 51(4):241-53 (2005)

  • [16]Butovsky O, Talpalar AE, Ben-Yaakov K, Schwartz M. Activation of microglia by aggregated beta-amyloid or lipopolysaccharide impairs MHC-II expression and renders them cytotoxic whereas IFN-gamma and IL-4 render them protective. Mol Cell Neurosci 29(3):381-93 (2005)

  • [17]Butovsky O, Ziv Y, Schwartz A. Microglia activated by IL-4 or IFN-gamma differentially induce neurogenesis and oligodendrogenesis from adult stem/progenitor cells. Mol Cell Neurosci 31(1):149-60 (2006)

  • [18]Shaked I, Porat Z, Gersner R. Early activation of microglia as antigen-presenting cells correlates with T cell-mediated protection and repair of the injured central nervous system. J Neuroimmunol 146(1-2):84-93 (2004)

  • [19]Dagkalis A, Wallace C, Hing B. CX3CR1-deficiency is associated with increased severity of disease in experimental autoimmune uveitis. Immunology 128(1):25-33 (2009)

  • [20]Egwuagu CE, Bahmanyar S, Mahdi RM. Predominant usage of V beta 8.3. Tcell receptor in a T cell line that induces experimental autoimmune uveoretinitis (EAU) Clin Immunol Immunopathol 65(2):152-60 (1992)

  • [21]Mizrahi T, Hauben E, Schwartz M. The tissue-specific self-pathogen is the protective self-antigen: the case of uveitis. J Immunol 169(10):5971-7 (2002)

  • [22]Ng TF, Streilein JW. Light-induced migration of retinal microglia into the subretinal space. Invest Ophthalmol Vis Sci 42(13):3301-10 (2001)

  • [23]Zhang C, Lei B, Lam TT. Neuroprotection of photoreceptors by minocycline in light-induced retinal degeneration. Invest Ophthalmol Vis Sci 45(8):2753-9 (2004)

  • [24]Ni YQ, Xu GZ, Hu WZ. Neuroprotective effects of naloxone against light-induced photoreceptor degeneration through inhibiting retinal microglial activation. Invest Ophthalmol Vis Sci 49(6):2589-98 (2008)

  • [25]Egwuagu CE, Mahdi RM, Nussenblatt RB. Evidence for selective accumulation of V beta 8+ T lymphocytes in experimental autoimmune uveoretinitis induced with two different retinal antigens. J Immunol 151(3):1627-36 (1993)

  • [26]Fauser S, Nguyen TD, Bekure K. Differential activation of microglial cells in local and remote areas of IRBP1169-1191-induced rat uveitis. Acta Neuropathol 101(6):565-71 (2001)

  • [27]Shahinfar S, Edward DP, Tso MO. Apathologic study of photoreceptor cell death in retinal photic injury. Curr Eye Res 10(1):47-59 (1991)

  • [28]Zhang C, Shen JK, Lam TT. Activation of microglia and chemokines in light-induced retinal degeneration. Mol Vis 11:887-95(2005)

  • [29]Egwuagu CE, Sztein J, Mahdi RM. IFN-gamma increases the severity and accelerates the onset of experimental autoimmune uveitis in transgenic rats. J Immunol 162(1):510-7 (1999)

  • [30]Zhang R, Qian J, Guo J. Suppression of experimental autoimmune uveoretinitis by Anti-IL-17 antibody. Curr Eye Res 34(4):297-303 (2009)

  • [31]Carlson SL, Parrish ME, Springer JE. Acute inflammatory response in spinal cord following impact injury. Exp Neurol 151(1):77-88 (1998)

  • [32]Dusart I, Schwab ME. Secondary cell death and the inflammatory reaction after dorsal hemisection of the rat spinal cord. Eur J Neurosci 6(5):712-24 (1994)

  • [33]Popovich PG, Guan Z, Wei P. Depletion of hematogenous macrophages promotes partial hindlimb recovery and neuroanatomical repair after experimental spinal cord injury. Exp Neurol 158(2):351-65 (1999)

  • [34]Rapalino O, Lazarov-Spiegler O, Agranov E. Implantation of stimulated homologous macrophages results in partial recovery of paraplegic rats. Nat Med 4(7):814-21 (1998)

  • [35]Hammarberg H, Lidman O, Lundberg C. Neuroprotection by encephalomyelitis: rescue of mechanically injured neurons and neurotrophin production by CNS-infiltrating T and natural killer cells. J Neurosci 20(14):5283-91 (2000)

  • [36]Faden AI. Pharmacological treatment of central nervous system trauma. Pharmacol Toxicol 78(1):12-7 (1996)

  • [37]Smith DH, Casey K, McIntosh TK. Pharmacologic therapy for traumatic brain injury: experimental approaches. New Horiz 3(3):562-72 (1995)

  • [38]David S, Bouchard C, Tsatas O, Giftochristos N. Macrophages can modify the nonpermissive nature of the adult mammalian central nervous system. Neuron 5(4):463-9 (1990)

  • [39]Moalem G, Leibowitz-Amit R, Yoles E. Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy. Nat Med 5(1):49-55 (1999)

  • [40]Hauben E, Agranov E, Gothilf A. Posttraumatic therapeutic vaccination with modified myelin self-antigen prevents complete paralysis while avoiding autoimmune disease. J Clin Invest 108(4):591-9 (2001)

  • [41]Muhallab S, Lundberg C, Gielen AW. Differential expression of neurotrophic factors and inflammatory cytokines by myelin basic protein-specific and other recruited T cells infiltrating the central nervous system during experimental autoimmune encephalomyelitis. Scand J Immunol 55(3):264-73 (2002)

  • [42]Schori H, Yoles E, Schwartz M. T-cell-based immunity counteracts the potential toxicity of glutamate in the central nervous system. J Neuroimmunol 119(2):199-204 (2001)

  • [43]Kipnis J, Mizrahi T, Yoles E. Myelin specific Th1 cells are necessary for post-traumatic protective autoimmunity. J Neuroimmunol 130(1-2):78-85 (2002)

  • [44]Ye F, Han L, Lu Q. Retinal self-antigen induces a predominantly Th1 effector response in Axl and Mertk double-knockout mice. J Immunol 187(8):4178-86 (2011)

  • [45]Avidan H, Kipnis J, Butovsky O. Vaccination with autoantigen protects against aggregated beta-amyloid and glutamate toxicity by controlling microglia: effect of CD4+CD25+ T cells. Eur J Immunol 34(12):3434-45 (2004)

  • [46]Arroul-Lammali A, Djeraba Z, Belkhelfa M. Early involvement of nitric oxide in mechanisms of pathogenesis of experimental autoimmune uveitis induced by interphotoreceptor retinoid-binding protein (IRBP) J Fr Ophtalmol 35(4):251-9 (2012)

  • [47]Garlipp MA, Nowak KR, Gonzalez-Fernandez F. Cone outer segment extracellular matrix as binding domain for interphotoreceptor retinoid-binding protein (IRBP) J Comp Neurol 520(4):756-69 (2012)

  • [48]Shaw NS, Noy N. Interphotoreceptor retinoid-binding protein contains three retinoid binding sites. Exp Eye Res 72(2):183-90 (2001)

  • [49]Schwartz M, Shaked I, Fisher J. Protective autoimmunity against the enemy within: fighting glutamate toxicity. Trends Neurosci 26(6):297-302 (2003)

  • [50]Nakajima K, Honda S, Tohyama Y. Neurotrophin secretion from cultured microglia. J Neurosci Res 65(4):322-31 (2001)

  • [51]Nakajima K, Tohyama Y, Kohsaka S, Kurihara T. Ability of rat microglia to uptake extracellular glutamate. Neurosci Lett 307(3):171-4 (2001)

  • [52]Piani D, Frei K, Do KQ. Murine brain macrophages induced NMDA receptor mediated neurotoxicity in vitro by secreting glutamate. Neurosci Lett 133(2):159-62 (1991)

  • [53]Piani D, Spranger M, Frei K. Macrophage-induced cytotoxicity of N-methyl-D-aspartate receptor positive neurons involves excitatory amino acids rather than reactive oxygen intermediates and cytokines. Eur J Immunol 22(9):2429-36 (1992)

  • [54]Bal-Price A, Brown GC. Inflammatory neurodegeneration mediated by nitric oxide from activated glia-inhibiting neuronal respiration, causing glutamate release and excitotoxicity. J Neurosci 21(17):6480-91 (2001)

  • [55]Chao CC, Hu S, Ehrlich L, Peterson PK. Interleukin-1 and tumor necrosis factor-alpha synergistically mediate neurotoxicity: involvement of nitric oxide and of N-methyl-D-aspartate receptors. Brain Behav Immun 9(4):355-65 (1995)

  • [56]Kitaoka Y, Munemasa Y, Nakazawa T, Ueno S. NMDA-induced interleukin-1beta expression is mediated by nuclear factor-kappa B p65 in the retina. Brain Res 1142:247-55 (2007)

  • [57]Chao CC, Molitor TW, Hu S. Neuroprotective role of IL-4 against activated microglia. J Immunol 151(3):1473-81 (1993)

  • [58]Downen M, Amaral TD, Hua LL. Neuronal death in cytokine-activated primary human brain cell culture: role of tumor necrosis factor-alpha. Glia 28(2):114-27 (1999)

  • [59]Tan J, Town T, Paris D. Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation. Science 286 (5448):2352-5 (1999)

  • [60]Butovsky O, Hauben E, Schwartz M. Morphological aspects of spinal cord autoimmune neuroprotection: colocalization of T cells with B7--2 (CD86) and prevention of cyst formation. FASEB J 15(6):1065-7 (2001)

  • [61]Liu B, Andrieu-Abadie N, Levade T. Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death. J Biol Chem 273(18):11313-20 (1998)

  • [62]Minghetti L, Levi G. Induction of prostanoid biosynthesis by bacterial lipopolysaccharide and isoproterenol in rat microglial cultures. J Neurochem 65(6):2690-8 (1995)

  • [63]Hauben E, Schwartz M. Therapeutic vaccination for spinal cord injury: helping the body to cure itself. Trends Pharmacol Sci 24(1):7-12 (2003)

  • [64]Popovich PG, Stuckman S, Gienapp IE, Whitacre CC. Alterations in immune cell phenotype and function after experimental spinal cord injury. J Neurotrauma 18(9):957-66 (2001)

  • [65]Banati RB, Graeber MB. Surveillance, intervention and cytotoxicity: is there a protective role of microglia? Dev Neurosci 16(3-4):114-27 (1994)

  • [66]Ling EA, Wong WC. The origin and nature of ramified and amoeboid microglia: a historical review and current concepts. Glia 7(1):9-18 (1993)

  • [67]Perry VH. A revised view of the central nervous system microenvironment and major histocompatibility complex class II antigen presentation. J Neuroimmunol 90(2):113-21 (1998)

  • [68]Roque RS, Imperial CJ, Caldwell RB. Microglial cells invade the outer retina as photoreceptors degenerate in Royal College of Surgeons rats. Invest Ophthalmol Vis Sci 37(1):196-203 (1996)

  • [69]Yang P, de Vos AF, Kijlstra A. Macrophages in the retina of normal Lewis rats and their dynamics after injection of lipopolysaccharide. Invest Ophthalmol Vis Sci 37(1):77-85(1996)

  • [70]Benveniste EN. Role of macrophages/microglia in multiple sclerosis and experimental allergic encephalomyelitis. J Mol Med (Berl) 75(3):165-73 (1997)

  • [71]Akaishi K, Ishiguro S, Durlu YK, Tamai M. Quantitative analysis of major histocompatibility complex class II-positive cells in posterior segment of Royal College of Surgeons rat eyes. Jpn J Ophthalmol 42(5):357-62 (1998)

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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

1 Jun 2016Review

Photoreceptor IRBP prevents light induced injury

Zhongcui Sun 1, Meng Zhang 1, Wei Liu 1, Jie Tian 1, Gezhi Xu 1,*
Affiliation
Article Info

1 Department of Ophthalmology, Eye and ENT Hospital, Fudan University, Shanghai, China

Abstract

Interphotoreceptor retinoid-binding protein (IRBP) is a classic inducer of experimental autoimmune uveoretinitis (EAU). Although IRBP causes neuronal loss in susceptible animals, resistant animals such as Sprague-Dawley (SPD) rats can benefit from the evoked protective autoimmune responses. The aim of the present study was to analyze the neuroprotective effects of IRBP against light-induced photoreceptor degeneration. We immunized 75 male SPD rats with IRBP and the rats were then exposed to blue light for 24hours (IRBP group). Seventy five rats were included in the control group. We found that the number of apoptotic cells in the outer nuclear layer (ONL) peaked on 1 day after light exposure, and the ONL thickness decreased significantly on day 3. OX42-positive cells appeared in the ONL immediately after light exposure, and their number peaked on day 3, and changed from resting ramified cells to activated amoeboid cells. Compared with the control group (n=75), the IRBP group showed less apoptotic cells, a thicker ONL, and reduced expression of tumor necrosis factor-alpha. These outcomes indicate the IRPB might protect retinal photoreceptors against light-induced injury.

Keywords

  • Photoreceptor
  • IRBP
  • Light
  • Injury
  • Cell Death
  • Review

References