The prevalence of allergy is rising globally at an alarming rate, which is currently at 20-40% of individuals in westernized nations. In the eye, allergic conditions can take on the acute form such as in seasonal and perennial allergic conjunctivitis, or a more severe and debilitating chronic form such as in vernal and atopic keratoconjunctivitis. Indeed, some key aspects of allergic eye disease pathophysiology are understood, such as the chief role of mast cells in the acute allergic reaction, and the contribution of eosinophils in late onset and chronic allergy. However, recent developments in animal models and clinical studies have uncovered new and important roles for previously underappreciated players, including chemokine receptors on ocular surface dendritic cells such as CCR7, histamine and leukotriene receptors on conjunctival goblet cells, and a role for mast cells in late-onset manifestations. Furthermore, recent work in animal models has now delineated the contribution of IL-4 in the increased incidence of corneal graft rejection seen in perioperative allergic conjunctivitis. Recent studies such as these mean that conventional paradigms and concepts should therefore be revisited. The aim of this review is to highlight the most recent advances and insights on newly appreciated players in the pathogenesis of allergic eye disease.

A light-scattering study has been made to investigate the effect of added styrene-butadiene diblock copolymer on the phase-separation kinetics of blends of low molecular weight polystyrene and polybutadiene. The scattered light intensity was measured at 2 O intervals up to 60' as a function of time from the beginning of phase separation into the late stage of Ostwald ripening. Various corrections, including the one for double scattering, were applied to the observed intensity. The effect of the added block copolymer was to retard the growth of phase-separated domains, as seen from the time evolution of qmw and I,, of the peak in the intensity curve. This can be explained in terms of the reduction in the interfacial tension between the demixed phases, resulting from accumulation of block copolymer there. The time-evolution exponents of qmu and I, , , the invariant Q, and the superposition of scattering intensity curves all show the validity of dynamic scaling in the late ripening stage.

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. Immediate hypersensitivity reactions in the conjunctiva are ablated in mice deficient in eotaxin-1, despite normal numbers of tissue mast cells and levels of IgE. To further define the co-stimulatory signals mediated by chemokine receptor 3 (CCR3), an eotaxin-1 receptor, effects of CCR3 blockade were tested with an allergic conjunctivitis model and in ex vivo isolated connective tissue-type mast cells. Our results show that CCR3 blockade significantly suppresses allergen-mediated hypersensitivity reactions as well as IgE-mediated mast cell degranulation. We propose that a co-stimulatory axis by CCR3, mainly stimulated by eotaxin-1, is pivotal in mast cell-mediated hypersensitivity reactions.

Background: CC chemokine ligand 2 (CCL2) recruits leukocytes in inflammatory tissues. Results: Vimentin, a cytoskeletal protein, interacted with phosphorylated MAPKs, was critical for CCL2 production in mast cells activated via F⑀cRI and a CC chemokine receptor. Conclusion: Vimentin was involved in optimal CCL2 production in mast cells. Significance: This work contributes to understanding of mechanisms for chemokine production in mast cells, which are therapeutic targets for allergic inflammation.