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Lupus
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Prolactin in murine systemic lupus erythematosus

R W McMurray

Rheumatology Section, GV (Sonny) Montgomery VA Hospital and the Division of Rheumatology and Molecular Immunology, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA; Division of Rheumatology and Molecular Immunology, L525 Clinical Sciences Building University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA Robert.McMurray{at}med.va.gov

Murine systemic lupus erythematosus (SLE) manifests several autoimmune perturbations that resemble human SLE, including cytokine aberrations, lymphoproliferation, hypergammaglobulinemia, autoantibody formation, and immune complex glomerulonephritis. In multiple studies, elevated serum prolactin concentrations (hyperprolactinemia) stimulated appearance or progression of murine lupus. Autoimmune disease acceleration by prolactin appears to be accentuated by estrogen stimulation of prolactin secretion and independent of immunosuppressive effects of androgens such as testosterone. Conversely, suppression of serum prolactin concentrations by bromocriptine inhibits development of murine SLE. These data clearly support the concept that prolactin is immunostimulatory in autoimmune disease and that the therapeutic goal of lowering serum prolactin concentrations may be beneficial to patients. Further utilization of murine SLE models will facilitate dissection of the actions and interactions of prolactin with estrogen, progesterone and testosterone and lead to a better understanding of hormonal immunomodulation and therapy of autoimmune disease.

Key Words: prolactin • mouse • bromocriptine

Lupus, Vol. 10, No. 10, 742-747 (2001)
DOI: 10.1191/096120301717164985
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This article has been cited by other articles:


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 LupusHome page
L.-y. Yu-Lee
Stimulation of interferon regulatory factor-1 by prolactin
Lupus, October 1, 2001; 10(10): 691 - 699.
[Abstract] [PDF]


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