Androgen control of secretory component mRNA levels in the rat lacrimal gland.

The functional expression of the secretory immune system of the eye is critically dependent upon secretory component (SC),1 the polymeric IgA receptor.2 This glycoprotein, which is produced by lacrimal gland epithelial cells, controls the transfer of secretory IgA (slgA) antibodies to the ocular surface, whereupon sIgA defends against microbial agents and toxic compounds.1 Given this pivotal role of SC in ocular mucosal immunity, our research has sought to elucidate the processes involved in the synthesis and secretion of this lacrimal protein. Such studies have demonstrated that: [a] SC production by rat lacrimal tissue displays distinct, gender-related differences (i.e. glands of males produce significantly more SC than those of females);3,4 and [b] SC synthesis by rat lacrimal acinar cells is uniquely regulated by the endocrine, nervous and immune systems.5.6 Thus, SC production is stimulated by androgens, vasoactive intestinal peptide (VIP), β-adrenergic agonists (e.g. isoproterenol), interleukm-lα (EL-lα), interleukin-1β (IL-Iβ), tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2), and suppressed by cholinergic agonists (e.g. carbachol choline). Moreover, these gender-associated and neuroendocrinimmune effects on lacrimal SC synthesis appear to be unique to the eye, given that SC production by other mucosal sites: [a] may show no sexual dimorphism (e.g. salivary, respiratory, intestinal, D.A. Sullivan, unpublished data); and [b] may be enhanced or inhibited, depending upon the tissue, by estrogens, progestins, glucocorticoids, prolactin, thyroxine, substance P and γ-interferon (γ-IFN),7–13 which agents have no demonstrable impact on the constitutive SC Output by lacrimal acinar cells.6