Abstract
Recent research in our laboratory and others has demonstrated keratoconjunctivitis sicca (KCS, dry eye) is caused by an autoimmune inflammatory process affecting the lacrimal “functional unit”. This is composed of the lacrimal glands (main and accessory), ocular surface and interconnecting innervation. The histological hallmark of this disease, regardless if an individual is diagnosed with systemic autoimmune syndrome or is subject to a local autoimmune event, is an immune cell infiltration of the lacrimal glands (main and accessory) as well as the conjunctival substantia propria and epithelium. The infiltrating cells are typically CD4-positive T-helper cells. They target the tissues in response to a local epithelial antigen presentation resulting from a neurogenic inflammation of the lacrimal glands and ocular tissues. This inflammation is facilitated by an age-related (menopause) or treatment-related (anti-androgen therapy) loss of circulating androgens in the affected tissues. The purpose of this study was to evaluate mouse models of autoimmunity to investigate initiation of the observed lacrimal gland and ocular surface inflammation and determine the role of ICAM-1 in the pathophysiology of dry eye.
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