Cell-adhesion molecules play a crucial role in a variety of immunological processes, including antigen presentation, cell-mediated cytolysis, immunoglobulin production, and lymphocyte homing. However, little is known about the contribution of cell-adhesion molecules in the induction of antigen-specific unresponsiveness. The present study examined the role of cell-adhesion molecules in the induction of a unique form of antigen- specific unresponsiveness, anterior chamber-associated immune deviation (ACAID). In vivo administration of monoclonal antibodies against leukocyte function antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) prevented the induction of ACAID. Hosts treated with either anti-ICAM-1 or anti-LFA-1 failed to develop regulatory cells that inhibited delayed-type hypersensitivity (DTH) responses to alloantigens. However, inhibition of ACAID was transient since mice were capable of developing ACAID 3 wk following cessation of antibody treatment. Flow-cytometry analysis of splenic lymphocytes revealed that the inhibitory effect of anti-cell-adhesion molecule antibodies was not due to depletion of CD4+, CD8+, or Thy 1.2+ T cells. The present findings indicate that LFA-1/ICAM-1 interactions are necessary for the induction of at least one regional immunoregulatory process, (i.e., ACAID).
|Original language||English (US)|
|Number of pages||6|
|Publication status||Published - 1994|
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