Secretory immune system of the male reproductive tract: effects of dihydrotestosterone and estradiol on IgA and secretory component levels

Transcriptional control of the murine polymeric IgA receptor promoter by glucocorticoids

“…Because glucocorticoid response elements are capable of binding to the androgen receptor, the identified element may account for the androgen responsiveness of pIgR in both prostate and in epithelial cells of the lacrimal gland (11,37). Dexamethasone responsiveness of pIgR is also tissue specific, since production is elevated in hepatocytes and salivary cells in a dose-and time-dependent manner, while decreasing in the mammary gland and cerviovaginal secretions (5,40,41).…”

Immunoglobulin Transport and Immunoglobulin Receptors

“…By contrast, pIgR expression in rabbit mammary gland is upregulated by prolactin and antagonized by estrogen and progesterone (Rosato et al, 1995). In the male reproductive tract, including the prostate and seminal vesicles, pIgR expression is upregulated by androgens (Stern et al, 1992). Interestingly, androgens also upregulate pIgR expression in the lacrimal gland of male rats, where SC output in tears is significantly higher than in female rats (Sullivan et al, 1984a;Vanaken et al, 1998).…”

“…However, IgA-containing plasma cells were detected only in the urethral gland in the bulbous part of the urethra and not at other sites where pIgR was present (Parr and Parr, 1989b). In another study, total levels of IgA and pIgR were measured by radioimmunoassay in reproductive tissues of the male rat (Stern et al, 1992). High levels of pIgR were detected in the prostate, presumably reflecting expression in the epithelium of the excretory ducts.…”

Hormones and Local Immunity

“…For example the effect of testos terone on lacrimal glands increases IgA, but not IgG, secretion, possibly by stimulating secretory component production [46,49]. These effects are mediated through the pituitary gland as the ablation of this organ leads to inhibition of testosterone-induced IgA secretion [49], In terestingly, in the reproductive tract of male rats, both estrogen and testosterone increased secretory component levels, without influencing IgA production [46], Andro genic steroids could also possibly modulate functional ac tivity of T cells since dehydroepiandrosterone (a weak androgenic steroid) enhanced production of IL-2 and y-IFN, but not IL-4, by activated T cells in vitro [69]. In contrast, the testosterone metabolite dihydrotestosterone (DHT) inhibited IL-4, IL-5 and y-IFN production stim ulated by anti-CD3 antibody-activated T cells [70].…”

“…In contrast others have shown that estrogen enhances only IgE-mediated but not SP-mediated histamine release from mast cells [37]. Ap parent estrogen receptors on rat peritoneal mast cells have recently been described using specific antireceptor antibody; however, estrogen alone does not have any ef fect on mast cell function [36], Estrogen can elevate antibody (IgM) production in re sponse to T-dcpcndcnt antigens [21,[38][39][40], enhance Tdependent B-ccll proliferation [41][42][43][44] and expression of surface immunoglobulins on plasma cells [45], It also has a pronounced effect on IgA transport in the genitourinary tract [46][47][48] and lacrimal gland [26,49] apparently by affecting the production of secretory component. Estro gen has a potentially dose-dependent dualistic effect as it has been shown to enhance (10"10M) or inhibit (10"' M) IL-6-induced IgM production by B cells [50].…”