Ablation of type I hypersensitivity in experimental allergic conjunctivitis by eotaxin-1/CCR3 blockade.

The immune response is regulated, in part, by effector cells whose activation requires multiple signals. For example, T cells require signals emanating from the T cell antigen receptor and co-stimulatory molecules for full activation. Here, we present evidence indicating that IgE-mediated hypersensitivity reactions in vivo also require cognate signals to activate mast cells.

Transcriptional analyses before and after suppression of immediate hypersensitivity reactions by CCR3 blockade in eyes with experimental allergic conjunctivitis.

Purpose: To characterize the transcriptome of allergic conjunctivitis mediated by eosinophil-related chemokine receptor CCR3 and to identify a candidate for possible therapeutic intervention in eosinophilic inflammation of the eye.

Methods: Mice were sensitized to ragweed pollen, and allergic conjunctivitis was induced by an allergen challenge. The induction of allergic conjunctivitis was used to determine whether an inhibition of CCR3 would suppress eosinophilic inflammation and the allergen-induced immediate hypersensitivity reaction.

Roles of chemokines in ocular allergy and possible therapeutic strategies.

The mechanism of ocular surface allergy in the forms of atopic conjunctivitis and vernal keratoconjunctivitis has been highlighted by specific functions of chemokines. In the context of late-phase allergic responses, these molecules have key roles in recruitment and activation of leukocytes. Their interaction with ligands is redundantly regulated; however, results from strategies to block subsets of chemokines have revealed unexpected or highly organized roles of these mediators.