McNamara Nancy A
Department of Anatomy, Francis I. Proctor Foundation, University of California San Francisco, San Francisco, CA 94143-0412, USA.
Optom Vis Sci. 2010 Apr;87(4):233-8. doi: 10.1097/OPX.0b013e3181c914ed.
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.
自身免疫介导的水样泪液缺乏的一个毁灭性后果是眼表的病理性角化。它由异常免疫反应引发，这种反应促进了黏膜上皮细胞分化改变的进程。角化性眼表疾病的治疗具有挑战性。局部治疗在急性加重期大多不足，而进展性疾病通常需要全身免疫抑制。有必要结合转化研究和基础科学研究来理解异常免疫与病理性角化之间的联系。我回顾了旨在开发控制或预防眼表角化的靶向治疗方法的最新研究和未来方向。
