Immune privilege in the anterior chamber of the eye is not extended to intraocular Listeria monocytogenes.

Resistance to many pathogens, such as Listeria monocytogenes, is correlated with the host's capacity to generate a ThI cell-mediated immune response in which delayed-type hypersensitivity (DTH) is activated. A wide variety of antigens induce down-regulation of DTH when introduced into the anterior chamber of the eye. This immunoregulatory phenomenon has been termed anterior chamber-associated immune deviation (ACAID) and is believed to be a primary mechanism for the immune privilege of the anterior chamber. Suppression of DTH, as a result of anterior chamber priming, could carry significant risk to the host's well-being as the resistance to many pathogens relies heavily on DTH-dependent ThI responses. Studies were performed to determine if a bacterial pathogen, L. monocytogenes, introduced into the anterior chamber of the eye would induce a down-regulation of systemic DTH. Intracameral inoculation of infectious L. monocytogenes into genetically susceptible C3H and BALB/c mice did not induce suppression of DTH, but instead resulted in a significant footpad swelling response to bacterial antigens. Likewise, intracameral inoculation of L. monocytogenes into genetically resistant C57BL/6 mice also induced vibrant bacterial-specific DTH. Using an in-vitro model of ACAID, we showed that macrophage suspensions that were simultaneously exposed to L. monocytogenes and bovine serum albumin (BSA) antigens, in the presence of aqueous humor (AH), induced listerial-specific DTH responses, yet simultaneously induced suppression of BSA-specific DTH. Collectively, the results indicate that immune privilege is not extended to all foreign antigens that enter the anterior chamber of the eye, and as a result, some intraocular antigens can provoke strong systemic DTH. However, non-ACAID-inducing antigens do not prejudice the down-regulation of DTH by other antigens which normally induce ACAID.