Prolactin as a modulator of lymphocyte responsiveness provides a possible mechanism of action for cyclosporine.
Lymphocyte responsiveness in rats was found to depend on serum prolactin levels. Blocking pituitary prolactin release with bromocriptine severely reduces lymphocyte reactivity in vitro (mixed lymphocyte reaction) as well as in vivo (graft-versus-host reaction). In addition, evidence for a prolactin/growth hormone-related mRNA species produced in mitogen- and antigen-stimulated lymphocytes has been obtained. Prolactin was shown to compete in a dose-dependent fashion with the immunosuppressant cyclosporine (cyclosporin A) for a common binding site on the surface of T lymphocytes. Further, stimulation of prolactin secretion reversed the immunosuppression induced by cyclosporine. We conclude that prolactin is involved in the maintenance of T-cell immunocompetence and that the immunosuppressive effects of cyclosporine may be mediated by the displacement of prolactin from binding sites on lymphocytes.
D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001667:Binding, Competitive; D003524:Cyclosporins / Q000494:pharmacology*; D005260:Female; D005434:Flow Cytometry; D006087:Graft vs Host Reaction; D006462:Hemolytic Plaque Technique; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D008214:Lymphocytes / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D011388:Prolactin / Q000502:physiology*; D051381:Rats
D003524:Cyclosporins; D011388:Prolactin