In recent years there has been increasing evidence in the literature that hormones are capable of regulating the immune system. There is evidence to suggest that prolactin is an immunostimulatory hormone and that reduction of serum prolactin levels in experimental animals by hypothesectomy or treatment with bromocriptine will result in a degree of immunosuppression. An animal model of experimental autoimmune uveitis (EAU) induced by immunization of rats with S-antigen (a soluble antigen from the retina) is used to study intraocular inflammatory disease. We have demonstrated a decrease in antibody production in both male and female rats and a decreased incidence of uveitis in female animals but no significant effect on the immune responses measured by lymphocyte proliferation. As reported before, high doses of cyclosporine (10 mg/kg) results in only partial reduction of intraocular inflammation. We have demonstrated that the suppression of prolactin by concurrent use of bromocriptine in combination with low dose cyclosporine is more effective than either drug separately in suppressing both the incidence of disease as well as cellular and humoral immune responses. Evidence in the literature suggests that cyclosporine competes with prolactin for binding sites on lymphocytes therefore reductions in prolactin level may reduce competition for those sites and make cyclosporine treatment more effective. Further studies with this animal model will elucidate other aspects of the neuroendocrine axis that may be utilized to regulate the immune system to treat autoimmune diseases.
