Long-term corneal allograft survival leads to an antigen-specific suppression of the delayed type hypersensitivity immune response and resembles the suppression of the delayed type hypersensitivity that is observed in ACAID .
Both ocular resident mesenchymal cells and peripheral tolerance of ACAID actively contribute to the regulation of immune responses via the generation of Tregs.
Streilein, "Anterior chamber associated immune deviation (ACAID): regulation, biological relevance, and implications for therapy," International Reviews of Immunology, vol.
Niederkorn, "Characterization of the suppressor cell(s) responsible for anterior chamber-associated immune deviation (ACAID) induced in BALB/c mice by P815 cells," The Journal of Immunology, vol.
Streilein, "Characterization of suppressor cells in anterior chamber-associated immune deviation (ACAID) induced by soluble antigen: evidence of two functionally and phenotypically distinct T-suppressor cell populations," Immunology, vol.
ACAID has been shown to suppress Th1 and Th2 effector mechanisms in an antigen-specific manner, even after the generation of the immune response (9).
Thus, ACAID could be adapted to induce tolerogenic immunotherapy in humans in cases of Th1 or Th2-induced inflammation.