This novel mechanism was revealed by strong evidence that all clinical signs of allergic conjunctivitis, stimulated expression of IL-33 by ocular epithelium, upregulated Th2 cell receptors ST2 and IL1RAP, as well as Th2 cytokine-dominant inflammation were only observed in EAC model of wild type BALB/c and MyD88+/+ mice, but not in Tlr4-d or MyD88−/− mice with the same treatment by SRW sensitization and ocular surface challenge (Figs 2, 3, 4). Here, IL1RL1 is linked to atopic conjunctivitis.