Molecular mechanisms of keratinizing ocular surface disease.
A devastating consequence of autoimmune-mediated, aqueous tear deficiency is pathological keratinization of the ocular surface. It is setoff by an aberrant immune response that promotes a program of altered mucosal epithelial cell differentiation. The management of keratinizing ocular surface disease is challenging. Topical therapies are largely inadequate for acute exacerbations, and progressive disease often requires systemic immunosuppression. A combination of translational and basic science research is necessary to understand the link between aberrant immunity and pathological keratinization. I review recent research and future directions aimed to develop targeted therapies that control or prevent ocular surface keratinization.
McNamara
Nancy A
NA
Department of Anatomy, Francis I. Proctor Foundation, University of California San Francisco, San Francisco, CA 94143-0412, USA. nancy.mcnamara@ucsf.edu
D000818:Animals; D015551:Autoimmunity; D003228:Conjunctiva / Q000378:metabolism* / Q000473:pathology; D003315:Cornea / Q000378:metabolism* / Q000473:pathology; D015352:Dry Eye Syndromes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005136:Eye Proteins / Q000378:metabolism*; D006801:Humans; D008679:Metaplasia
D005136:Eye Proteins; C042434:tear proteins