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Cutting Edge: Lupus Susceptibility Interval Sle3/5 Confers Responsiveness to Prolactin in C57BL/6 Mice¹

Elena Peeva^*, Juana Gonzalez^*, Ruthmarie Hicks^* and Betty Diamond^2,

^* Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461; and Department of Medicine and Microbiology, Columbia University Medical Center, New York, NY 10032

Prolactin is of interest in the pathogenesis of systemic lupus erythematosus (SLE) because almost 25% of SLE patients display hyperprolactinemia, and serum prolactin correlates with disease activity in some patients. Furthermore, hyperprolactinemia causes early mortality in lupus-prone mice and induces a lupus-like phenotype in nonspontaneously autoimmune mice. We show here that the immunomodulatory effects of prolactin are genetically determined; hyperprolactinemia breaks B cell tolerance and causes a lupus-like serology in BALB/c mice expressing a transgene encoding the H chain of an anti-DNA Ab but not in C57BL/6 transgenic mice. In C57BL/6 mice that express both the H chain transgene and the lupus susceptibility interval Sle3/5, prolactin induces increased serum titers of anti-DNA Ab and glomerular Ig depositions. The increase in costimulation due to prolactin-mediated up-regulation of both CD40 on B cells and CD40L on T cells would appear to play a central role in lupus induction in this model.