Purpose: To review the recent exploration of the role of prolactin in immune function.
Materials and methods: Studies published that were identified through a MEDLINE search as well as through the bibliographies of those articles enumerated.
Results: Both humoral and cell-mediated immunity are compromised in hypophysectomized rats. The reintroduction of prolactin to these animals restores their immune function. Prolactin receptors have been identified on the membranes of white blood cells; furthermore, lymphocytes have been shown to secrete prolactin. Cyclosporin A directly competes with prolactin for binding to these receptors. This may be one mechanism of the immunosuppressive action of cyclosporin A. In addition to diminished levels, prolactin excess may also result in immunocompromise. This has been demonstrated in lactating female and prolactin-treated male rats, as well as hyperprolactinemic humans. Finally, prolactin abnormalities have been described in a number of immunologic disorders, including systemic lupus erythematosus, adjuvant arthritis, experimental allergic encephalomyelitis, and autoimmune uveitis and thyroid disease. Dopaminergic agents that suppress serum prolactin are now being used in clinical trials to treat a number of autoimmune diseases and to prevent rejection in organ transplant recipients.
Conclusion: At physiologic levels, prolactin is trophic for lymphocytes. Either too much, or too little, prolactin may be immunosuppressive. Lymphocytes produce a prolactin-like substance. Prolactin may play a role in a number of autoimmune processes.