Abstract

The ocular surface appears to be protected from bacterial and viral pathogens by polymeric IgA antibodies.1 These antibodies, which are produced by plasma cells in the lacrimal gland, bind to secretory component (SC) in the basolateral membrane of acinar epithelial cells, and are then transported to the apical membrane and secreted into tears.2 Of interest, the lacrimal secretion of sIgA, as well as free SC, appears to be significantly influenced by gender and hormones from the hypothalamic-pituitary-gonadal axis.2 Thus, almost 10 years ago, it was found that the concentrations of free SC and IgA in the tears of male rats were 2 to 5-fold higher than those in tears of female rats. These gender-associated differences in tear SC and IgA were shown to be caused by androgens.2 For example, castration led to a significant reduction in SC levels in tears of males, while having no impact on SC content in tears of females. In addition, administration of testosterone for 4 days to castrated male or female rats significantly increased tear SC levels. These studies showed that exposure of castrated rats to androgens resulted in alterations of lacrimal SC production.2 Moreover, later experiments demonstrated that this androgen control of SC, as well as IgA, is modulated by factors from the hypothalamus and pituitary.2 However, this research did not address whether androgens act directly on lacrimal tissue to change SC or IgA, or indirectly via an androgen-sensitive site, which in tum acts to modulate lacrimal SC and IgA.

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