Fibrosis in ocular allergic inflammation: recent concepts in the pathogenesis of ocular allergy.

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Mast cells and eosinophils are the main effector cells in allergic inflammation, but there is now compelling evidence that fibroblasts are also important players in the inflammatory response. In fact, they respond to different stimuli and release several mediators that modulate mast-cell and eosinophil functionality. In several allergic conditions such as vernal keratoconjunctivitis, asthma and atopic dermatitis the chronic presence of the inflammatory process has been associated with fibrosis and tissue remodeling, which in turn could cause irreversible alterations in the organ anatomy and functions. This review will discuss current advances in mast cell, eosinophil and fibroblast interactions in terms of their importance in the perpetuation of allergic inflammation and in contributing to the fibrosis and/or remodeling process in ocular allergy. As a main example of allergic ocular diseases associated with fibrosis, vernal keratoconjunctivitis is discussed in the light of recent findings. Several studies have recently shown that fibroblasts can modulate the functions of mast cells and eosinophils through the membrane form of stem cell factor and granulocyte-macrophage colony-stimulating factor, respectively. On the other hand, fibroblasts can be affected by inflammatory mediators derived from mast cells and eosinophils, such as transforming growth factor beta and nerve growth factor and by the T helper type 2 cytokines, IL-4 and IL-13, and vernal keratoconjunctivitis-derived fibroblasts display altered functions. Considerable useful information has been gained about the role of mast cells, eosinophils and fibroblasts in the perpetuation of allergic inflammation and tissue fibrosis and/or remodeling in general, and specifically in ocular allergy.