Role of inflammatory cytokines in induction of anterior chamber-associated immune deviation.

PURPOSE: To determine the extent to which proinflammatory cytokines [(interleukin-I-beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), gamma-interferon (gamma-IFN)] interfere with induction of anterior chamber-associated immune deviation (ACAID).
METHODS: Proinflammatory cytokines were injected intracamerally prior to local injection of ovalbumin (OVA), or added to cultures containing peritoneal exudate cells (PEC), transforming growth factor-beta (TGF beta), and OVA. After incubation, these cells were washed and injected intravenously into naive, syngeneic mice. One week later, the mice were immunized with OVA in adjuvant, and delayed hypersensitivity (DH) was assessed seven days later.
RESULTS: Eyes pretreated with IL-1 beta, TNF alpha or gamma-IFN failed to support ACAID induction. In addition, IL-1 beta and gamma-IFN robbed OVA-pulsed, TGF beta-treated PEC of their ability to induce ACAID, whether the inflammatory cytokines were added prior to, simultaneously with, or after exposure to TGF beta. By contrast, in-vitro exposure of PEC to TNF alpha was unable to prevent TGF beta-promoted ACAID.
CONCLUSION: IL-1 beta, gamma-IFN, and TNF alpha injected intracamerally rob the eye of immune privilege and prevent ACAID induction. In the cases of IL-1 beta and gamma-IFN, ACAID seems to be prevented by a direct action of the cytokines on antigen-presenting cells (APCs). In the case of TNF alpha, prevention of ACAID in vivo probably occurs by an APC-independent mechanism.