May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Ocular immune privilege regulates the innate/adaptive immune interface
Author Affiliations & Notes
  • A.W. Taylor
    Schepens Eye Research Institute, Boston, MA
    Ophthalmology, Harvard Medical School, Boston, MA
  • D. Yee
    Schepens Eye Research Institute, Boston, MA
  • Footnotes
    Commercial Relationships  A.W. Taylor, Schepens Eye Reseach Institute P; D. Yee, None.
  • Footnotes
    Support  NIH Grant EY10752
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 589. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      A.W. Taylor, D. Yee; Ocular immune privilege regulates the innate/adaptive immune interface . Invest. Ophthalmol. Vis. Sci. 2004;45(13):589.

      Download citation file:

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

  • Supplements

Abstract: : Purpose: The induction of inflammatory immunity requires the activation of antigen presenting cells (APC) by innate immune responses involving Toll–like receptors (TLR). Since, we have previously demonstrated that the immunosuppressive factors in aqueous humor suppress TLR4 (endotoxin) induced inflammatory activities, we have begun to examine the possibility that the immunosuppressive factors of normal aqueous humor can influence TLR–mediated APC activation of Th1 cells. Methods: Adherent mouse spleen cells (APC) were treated with 30 pg/ml of the immunosuppressive aqueous humor factor alpha–melanocyte stimulating hormone (α–MSH) for 20 minutes. Antigen, ovalbumin (OVA), and an activator of a specific TLR were added to the cultures. The APC were stimulated through TLR4 with E. coli lipopolysaccharide; through TLR2 with S. aureus cell walls; through TLR3 with polyI:C; and through TLR9 with purified E. coli DNA. The APC were incubated overnight, washed, and OVA–specific Th1 cells were added. The cultures were incubated for 48 hours and the supernatants were assayed for IFN–γ by ELISA. Results: Without TLR stimulation, the OVA–pulsed APC weakly stimulated IFN–γ production by the OVA–specific Th1 cells, and APC treatment with α–MSH did not alter this nominal activity. The TLR4–stimulated OVA–pulsed APC induced the Th1 cells to produce 3 to 5–fold greater amounts of IFN–γ, and α–MSH treatment of the APC completely suppressed this enhanced activity. In contrast, TLR2 and TLR9 stimulated APC suppressed the production of IFN–γ by the Th1 cells to below the amount of IFN–γ produced when using non–TLR stimulated APC, and α–MSH treatment of the APC did not enhance this suppression. Stimulating TLR3 had no effect on APC stimulation of IFN–γ production by the Th1 cells. Conclusion: The mechanisms of immunosuppression within the ocular microenvironment mediated by α–MSH include a selective regulation of immunity associated with specific TLR activation of APC. The implications of these findings are that the ocular microenvironment has separate mechanisms to suppress induction and activation of inflammatory immunity.

Keywords: immunomodulation/immunoregulation • immune tolerance/privilege • inflammation 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.