Abstract

Keratoconjunctivitis sicca (KCS), or dry eye syndrome, is characterized by the development of ocular surface damage. KCS can occur as an individual phenomenon, or in association (as a secondary phenomenon) with various types of systemic autoimmune disorders. Sjogren’s syndrome (SS), with the signature symptoms of dry eye and dry mouth, has the strongest association with KCS. The most prominent characteristic of SS is a progressive, follicular, lymphoid infiltration found in biopsy specimens of the lacrimal and salivary glands. These infiltrates consist of primarily CD4+ T cells and B cells demonstrated by immunohistological staining. Functional studies have shown that this type of impairment of the lacrimal gland results in decreased tear secretion and altered tear protein composition.1

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