April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Specific T Cell Mediated Immune Responses Do Not Play a Role in the Pathogenesis of Proliferative Vitreoretinopathy Induced by Dispase
Author Affiliations & Notes
  • Q. Gao
    State Key Lab Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China
  • W. Zhang
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio
  • J. tan
    State Key Lab Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China
  • P. Lehmann, V
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio
  • J. ge
    State Key Lab Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China
  • Y. duan
    State Key Lab Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China
  • W. li
    State Key Lab Ophthalmology, Zhongshan Ophthalmic Center, Guangzhou, China
  • Footnotes
    Commercial Relationships  Q. Gao, None; W. Zhang, None; J. tan, None; P. Lehmann, V, None; J. ge, None; Y. duan, None; W. li, None.
  • Footnotes
    Support  NSFC(national natural science foundation of china) Grant 30610337
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2710. doi:
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      Q. Gao, W. Zhang, J. tan, P. Lehmann, V, J. ge, Y. duan, W. li; Specific T Cell Mediated Immune Responses Do Not Play a Role in the Pathogenesis of Proliferative Vitreoretinopathy Induced by Dispase. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2710.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Proliferative vitreoretinopathy (PVR) is the leading cause of failure of surgery for rhegmatogenous retinal detachment. Although a great deal of information supports the role of the immune system in the development of PVR, the role of the immune system in the pathogenesis of PVR is still unclear. The purpose of this study is to determine the role of specific immune system on PVR using the Rag-1 gene knockout (KO) mice.

Methods: : PVR model was induced by 3µL dispase intravitreal injections at the concentration of 0.2 U/µL in 4-6 week Rag-1 gene knockout (B6.129S7-Rag1tmiMom/J mice)and wild type (WT) mice. The model eyes were examined and assessed including corneal, lens opacities, intravitreal hemorrhage and the fundus at the first, second, fourth, sixth and eighth weeks after intravitreal injection with a surgical microscope. Enzyme-linked Immunospot (ELISPOT) and intracellular staining for INF-γ and IL-2, Electroretinograms (ERG), Haematoxylin-Eosin (HE) staining and Immunofluorescence analysis were also performed at each time point. The model eyes were collected for histological and immunofluorescence analysis at 0hr,4hr,8hr,12hr,24hr,48hr ,5day and 7day.

Results: : Intravitreal injection of dispase in KO mice and WT mice induced a PVR-like condition. The PVR incidence,pathological changes and ERG result of model eyes in KO and WT mice have no obvious difference. Early Inflammatory infiltration occurs at the same speed in WT and KO mice, and T cells along with cells of the innate immune system (Microphage, NK cells) in WT mice. The ELISPOT and intracellular staining data showed no auto-antigen specific T cells response after the PVR induction.Conclusion Specific T cells mediated immune responses do not play a role in the pathogenesis of proliferative vitreoretinopathy induced by dispase.

Keywords: proliferative vitreoretinopathy • immune tolerance/privilege 
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