December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Ocular Immune Deviation to an Endogenous Retinal Protein
Author Affiliations & Notes
  • DS Gregerson
    Ophthalmology University of Minnesota Minneapolis MN
  • C Dou
    Ophthalmology University of Minnesota Minneapolis MN
  • Footnotes
    Commercial Relationships   D.S. Gregerson, None; C. Dou, None. Grant Identification: NIH Grant EY11542
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1954. doi:
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      DS Gregerson, C Dou; Ocular Immune Deviation to an Endogenous Retinal Protein . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1954.

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

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Abstract

Abstract: : Purpose: Current studies of ocular immune deviation, or ACAID (anterior chamber associated immune deviation), use the intraocular injection of antigen to induce the deviated immune responses. Virtually all studies are done in mice, where the small size of the eye magnifies the potential confounding effects of the injection protocol. Also, inoculation of a bolus of antigen is unlike that of an endogenous antigen, which would be present continuously, and probably at lower concentrations. We have used transgenic mice to look for the presence of immune deviation to an endogenous, intracellular retinal antigen. Methods: Transgenic mice which express beta-galactosidase in the photoreceptor cells of the retina and various other transgenic and non-transgenic control mice were immunized with beta-galactosidase. Seven days later, the mice were tested for immune responsiveness to beta-galactosidase by ear testing for DTH (delayed type hypersensitivity) and with in vitro proliferation assays. Spleen cells from transgenic mice were also transferred to normal recipients to test for the ability to transfer endogenous immune deviation. Results: Beta-galactosidase can induce immune deviation following intraocular inoculation in conventional ACAID-like fashion. More importantly, in mice with endogenous retinal beta-galactosidase expression, both the DTH response and proliferation assays to beta-galactosidase were depressed, despite immunization with beta-galactosidase. The ability to depress DTH was transferred by naïve spleen cells from transgenic mice to non-transgenic mice. Conclusion: Using the transgenic mice we show that an endogenous neo-self retinal antigen is able to induce immune deviation without intraocular injection. These results show that the intraocular inoculation protocols are not required for immune deviation, and that normal retinal proteins may exist in a state of endogenous immune deviation.

Keywords: 301 ACAID • 435 immunomodulation/immunoregulation • 433 immune tolerance/privilege 
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