Interleukin-1 abrogates anterior chamber-associated immune deviation.

Alloantigens placed into the anterior chamber of the eye elicit antigen-specific suppression of systemic delayed-type hypersensitivity (DTH) responses and severe impairment of skin allograft rejection. This pattern of immunologic alteration has been termed anterior chamber-associated immune deviation (ACAID) and is the underlying mechanism responsible for immunologic privilege within the anterior chamber of the eye. Previous studies indicate that the immunologic privilege associated with the anterior chamber of the eye might be the result of a deficiency of interleukin-2 (IL-2) during antigen presentation. The present study examined the role of IL-1 in the induction of ACAID. It is well known that intracameral (IC) inoculation of DBA/2 mastocytoma cells (P815) into allogeneic BALB/c recipients results in antigen-specific suppression of DTH responses and progressive tumor growth. The authors found, however, that sublines of P388D1 (DBA/2 monocyte/macrophage tumor) that produce IL-1 not only do not grow progressively in the anterior chamber, but also they can prevent the suppression of DTH (P less than or equal to 0.01). The role of IL-1 in the abolition of ACAID was confirmed in studies with IC-inoculated P815 cells. Systemic administration of exogenous IL-1 (by subcutaneous miniosmotic pumps) prevented the induction of ACAID in hosts that received IC inocula of P815 cells (P less than or equal to 0.01). These results indicate that induction of ACAID and perhaps the immune-privileged character of the anterior chamber is dependent on an IL-1 deficiency during the processing of IC alloantigens.