Induction of anterior chamber-associated immune deviation (ACAID) by allogeneic intraocular tumors does not require splenic metastases.

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Abstract
Anterior chamber-associated immune deviation (ACAID), induced by intracameral injection of allogeneic tumor cells, is expressed in three distinct ways: 1) progressive growth of intraocular tumors, 2) specific suppression of systemic allograft immunity, and 3) transient growth of allogeneic tumors injected subcutaneously. Induction of ACAID requires that alloantigen presentation occur via the anterior chamber; injection by other routes failed to elicit this phenomenon. Antigenic material must remain in the anatomically intact eye for at least 10 days; removal of the injected dye before this time prevented the establishment of ACAID. The similar temporal requirement for an anatomically intact spleen confirms the validity of the concept of a camero-splenic axis for processing of intracamerally injected alloantigens. Deployment of an alternate model of ACAID, using LP/J mice injected intracamerally with B16F10 melanoma, showed the antigen-specific inductive signal for ACAID (transmitted via the camero-splenic axis) was not in the form of viable alloantigen-bearing tumor cells that metastasize to the spleen. B16F10 melanoma cells were never found in the spleens or any other extraocular sites after intracameral injection, despite the fact these mice manifested ACAID and harbored enormous ocular tumors. The data emphasize that intraocular processing of antigens is a unique and dynamic phenomenon with significant, systemic immunologic consequences.