The injection of antigen into the anterior chamber (AC) of the eye results in a pattern of systemic immune responses termed anterior chamber associated immune deviation (ACAID). ACAID is characterized by down-regulation of delayed-type hypersensitivity (DTH) by T suppressor cells with normal antibody production and cytotoxic T cell responses. To better understand the mechanisms of ACAID, we studied the genetic restrictions and intraocular T cell interactions in TNP-ACAID. We report that (a) antigen is not reprocessed by the eye for the induction of suppression in TNP-ACAID, (b) the T cells injected into the AC and the recipient animal must match at genes in the immunoglobulin heavy chain (IgH) region of chromosome XII for TNP-ACAID to be induced, (c) TNP-coupled Lyt-1+, I-J+ T cells present antigen to viable T cells within the eye to induce systemic suppression, (d) although there is an IgH restriction between the T cells injected into the AC and the recipient, the interaction between the T cell antigen-presenting cell and the Tsi-cells in the AC inoculum is restricted to the I-J portion of the major histocompatibility complex, and (e) the two Tsi-cells that initiate the suppressor cascade have different antigen presentation requirements. These results further emphasize the complex interaction between T cells, which serves to control immune reactions in the eye.
|Number of pages||7|
|State||Published - Jul 1 1988|