September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Mechanisms of immune deviation
Author Affiliations & Notes
  • Jerry Y Niederkorn
    Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Footnotes
    Commercial Relationships   Jerry Niederkorn, None
  • Footnotes
    Support  Supported by NIH grants EY007641, EY005631, and EY020799 and Research to Prevent Blindness.
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Jerry Y Niederkorn; Mechanisms of immune deviation. Invest. Ophthalmol. Vis. Sci. 2016;57(12):No Pagination Specified.

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

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Presentation Description : The notion that they eye possessed a unique regulation of immunity and inflammation was recognized over 140 years ago and is termed “immune privilege”. The past 50 years have witnessed an explosion in the amount of information about the immune response in the eye. In particular, studies in rodents have revealed that multiple anatomical, physiological, and immunoregulatory mechanisms prevent the induction and expression of both adaptive and innate immune responses in the eye. Cell membrane molecules induce apoptosis of lymphocytes that enter the eye. Other cell membrane molecules inactivate the complement cascade in the eye. The aqueous humor of the eye contains a myriad of soluble anti-inflammatory and immunosuppressive molecules that silence both adaptive and innate immune responses. Antigens, including those expressed by viral pathogens, induce a unique form of immune deviation after entering anterior chamber of the eye. This anterior chamber-associated immune deviation (ACAID) down-regulates delayed-type hypersensitivity (DTH), cytotoxic T lymphocyte (CTL), and complement fixing antibody responses that are crucial for protecting against viral infections. However, immune privilege in the eye is not an all or none proposition. Some viral infections, such as herpes simplex virus (HSV) infections of the cornea circumvent immune privilege and elicit robust adaptive immune responses that eliminate the offending virus, but in the process blind the eye. In this case immune privilege is terminated to preserve life even at the cost of blindness. That is, hosts incapable of mounting adaptive immune responses to corneal infection with HSV die from viral encephalitis. Thus, immune deviation protects the eye from the damaging effects of immune-mediated inflammation to nominal antigens that pose no threat to the host’s survival. However, immune privilege is terminated when the immune apparatus senses “danger” and as a result, the full array of immune responses are marshaled to eliminate the infectious agent. Viral infections arising in the eye that fail to evoke “danger” signals benefit from immune deviation and the permissive ocular environment and thus, pose an existential threat to the host.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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