April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Ocular Immune Consequences Post Traumatic Brain Injury
Author Affiliations & Notes
  • R. Mathew
    Immunology, Schepens Eye Research Institute, Boston, Massachusetts
  • K.-S. Cho
    Immunology, Schepens Eye Research Institute, Boston, Massachusetts
  • D. F. Chen
    Immunology, Schepens Eye Research Institute, Boston, Massachusetts
  • J. Stein-Streilein
    Immunology, Schepens Eye Research Institute, Boston, Massachusetts
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5165. doi:
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    • Get Citation

      R. Mathew, K.-S. Cho, D. F. Chen, J. Stein-Streilein; Ocular Immune Consequences Post Traumatic Brain Injury. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5165.

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Abstract

Purpose: : As an extension of our previous work that showed that Retinal Laser Burn (RLB) to one eye abrogated immune privilege in both the burned and the non burned eye, we tested if injury to other areas of the brain might interfere with ocular immune privilege. Preliminary data showed that optic nerve crush also abrogated the ability to induce Anterior Chamber Associated Immune Deviation (ACAID) in both eyes. We next tested if an injury to a more distant site in the Central Nervous System (CNS) might interfere with immune privilege.

Methods: : A wound (no more than one mm depth) was induced in the right brain cortex (Traumatic Brain Injury) in C57BL/6 mice. Following injury, antigen was inoculated at various time points into the eye that was either ipsilateral or contralateral to the wound. Seven days later, the mice were immunized subcutaneously with the same antigen in Complete Freund's Adjuvant (CFA). One week later, the mice were assessed for their ability to develop Delayed Hypersensitivity (DH).

Results: : Mice without injury showed a classic suppression of DH post induction of ACAID. Mice that received Traumatic Brain Injury (TBI) showed no suppression of DH post injection of antigen into the eye, demonstrating a loss of immune privilege. Furthermore the mice did not recover their ability to develop immunological tolerance via the eye 21 days post TBI.

Conclusions: : In this study, we show that injury in non-ocular sites of the brain abrogates ocular immune privilege. Since there were no obvious signs of injury or inflammation in the eyes post TBI, we postulate that neuronal signals emanating from the injured brain site might be the responsible neuroinflammatory mediators that interfere in ocular mechanisms of immune privilege. This research was supported in part by NIH grant: EY011983

Keywords: immune tolerance/privilege • trauma • ACAID 
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