May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Contribution of Neuroretinal and Pigmented Epithelial Cell Factors to Subretinal Immunity
Author Affiliations & Notes
  • C.H. Lau
    Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical School, Boston, MA
  • A.W. Taylor
    Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical School, Boston, MA
  • Footnotes
    Commercial Relationships  C.H. Lau, None; A.W. Taylor, None.
  • Footnotes
    Support  NIH Grant EY10752 and Department of Defense/USAMRMC
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 970. doi:
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      C.H. Lau, A.W. Taylor; Contribution of Neuroretinal and Pigmented Epithelial Cell Factors to Subretinal Immunity . Invest. Ophthalmol. Vis. Sci. 2005;46(13):970.

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

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Abstract

Abstract: : Purpose:Previous studies by Streilein et al. revealed that the subretinal space is an immunosuppressive microenvironment. Since both the neuroretinal cells (NR) and the pigmented epithelial cells (RPE) have the potential to contribute factors into the subretinal space, we investigated the expression of cytokines produced by the NR and RPE and their effect on inflammatory macrophage activity. Methods: RPE eyecups and NR from healthy C57BL/6J mice were prepared and cultured for 24 hours. The eyecup supernatant (RPE–SN) and NR conditioned media (NR–SN) were transferred to macrophage cultures with or without lipopolyssacharide activation. After 48 hours culture, the macrophage culture supernatants were analyzed using a Bio–Rad multiplex analyzer for IL–1ß, IL–6, Il–10, IL–12 (p70), TNF–α, G–CSF, GM–CSF, MIP–1α, RANTES and KC. The RPE–SN and NR–SN were also analyzed by the multiplex analysis. Results: We found IL–6, IL–10, TNF–α, GM–CSF and KC in RPE–SN, and G–CSF and KC in the NR–SN. In the presence of resting macrophage, KC levels were reduced in both RPE–SN and NR–SN. RPE–SN suppressed G–CSF, while NR–SN increased GM–CSF production by resting macrophage. For LPS–activated macrophages, the RPE–SN did not suppress any LPS–induced factor, but did induce significant production of IL–10. The NR–SN significantly promoted TNF–α production, and significantly suppressed IL–1ß production by the activated macrophages. Conclusions:Both RPE and NR supernatants did not activate the macrophages; however, RPE–SN and NR–SN had differential effects on LPS–activated macrophages. Therefore neuroretinal and RPE cells contribute differently to the subretinal microenvironment. This implies that the mechanism of immunosuppression observed in the subretinal space is a combined effort of the RPE and neuroretina.

Keywords: immunomodulation/immunoregulation • inflammation • cytokines/chemokines 
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