Effect of anterior chamber-associated immune deviation (ACAID) on rat islet allograft rejection

Anterior chamber-associated immune deviation (ACAID) is characterized by the systemic inhibition of delayed type hypersensitivity (DTH) reactions to antigens which have previously been placed into the anterior chamber of the eye. Since its initial characterization, ACAID has been elicited to a wide variety of antigens, including alloantigens, and has been shown to be due to the immune deviating effects of factors such as transforming growth factor beta (TGF-beta) in the aqueous humor on ocular antigen-presenting cells (APCs). ACAID can also be induced by injecting animals with nonocular APCs, such as peritoneal exudate cells (PECs), which have been precultured with TGF-beta and antigen in vitro. The objective of this study was to determine whether alloantigenic ACAID can be effective in preventing the rejection of rat islet allografts. The notion that islet allograft rejection can be inhibited by ACAID stems from an early study showing an ACAID-induced delay in the rejection of skin grafts. Furthermore, the immune cells mediating a DTH reaction are similar to those implicated in islet allograft rejection, suggesting that they, too, may be subject to inhibition by ACAID. Our results showed that in spite of successful ACAID induction to islet allografts, recipient rats consistently rejected their grafts. Cytotoxic T cell activity (which is not inhibited by ACAID) directed against donor alloantigens was high in these animals and may have accounted, in part, for graft failure.