Purpose of review: This review highlights recent findings regarding the immune regulation of allergic conjunctivitis. Mouse models have facilitated prospective studies that have not been possible in patients. The availability of gene knockout mice and the wealth of monoclonal antibodies have permitted exquisite dissection of the pathophysiology and immune regulation of allergic conjunctivitis.
Recent findings: New insights have emerged in three areas: role of costimulatory molecules in the induction of Th2 immune responses; crucial role of IFN-gamma in the expression of allergic conjunctivitis; and the function of T regulatory cells in shaping conjunctival inflammation once the immune response has been initiated.
Summary: Allergic conjunctivitis involves early phase and late phase reactions. The early phase reaction is IgE antibody-dependent, whereas the late phase reaction is IgE-independent and is mediated by inflammatory cells, especially eosinophils. Recent studies on mouse models of allergic conjunctivitis have provided important insights into the immune regulation of both the early phase reaction and late phase reaction of allergic conjunctivitis. Mounting evidence suggests that IFN-gamma is crucial for optimum expression of allergic conjunctivitis. Costimulatory molecules influence the induction of Th2 immune responses and the early phase reaction, whereas regulatory T cells shape the expression of the late phase reaction of allergic conjunctivitis.