Abstract
Certain similarities exist in the pathophysiological processes and clinical features of advanced stages of various inflammatory ocular surface diseases, suggesting that common pathways contribute to these diseases. In this article, common pathways are analyzed with a focus on the role of the physiological resident mucosal immune system of the ocular surface, termed eye-associated lymphoid tissue (EALT). This is physiologically protective but if it is deregulated it can mediate an inflammatory immune answer. Common events in inflammatory ocular surface disease lead to a vicious circle of immune-modulated inflammation, with degenerative remodeling and loss of function.
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