Prolactin enhances the in vitro production of IgG in peripheral blood mononuclear cells from patients with systemic lupus erythematosus but not from healthy controls

doi:10.1136/ard.60.3.242

Annals of the Rheumatic Diseases 2001;60:242-247; doi:10.1136/ard.60.3.242

Ann Rheum Dis 2001;60:242-247 ( March )

Extended report

Prolactin enhances the in vitro production of IgG in peripheral blood mononuclear cells from patients with systemic lupus erythematosus but not from healthy controls A M Jacobi^a, W Rohde^b, H-D Volk^c, T Dörner^a, G-R Burmester^a, F Hiepe^a

^a Department of Medicine, Charité University Hospitals Berlin, Germany, ^b Institute of Experimental Endocrinology, Charité University Hospitals Berlin, Germany, ^c Institute of Medical Immunology, Charité University Hospitals Berlin, Germany

Correspondence to: Professor Dr med F Hiepe, Medizinische Klinik mit Schwerpunkt, Rheumatologie und Klinische Immunologie, Universitätsklinikum Charité, Humboldt-Universität, Schumannstr 20/21, D-10117 Berlin, Germany falk.hiepe@charité.de

Accepted for publication 28 July 2000

OBJECTIVES $---$ Recent evidence suggests that prolactin (PRL) plays a part in the pathogenesis of systemic lupus erythematosus (SLE). BecauseB cell hyperreactivity and autoantibodies are characteristic hallmarksof SLE, this study aimed at assessing the impact of this pituitaryhormone on IgG production by stimulating peripheral blood mononuclearcells (PBMC) withPRL.
METHODS $---$ PBMC from 11 patients with SLE assessed by the ECLAM score and eight healthy controls were incubated with PRL and culturedfor seven days. IgG production was measured by enzyme linked immunosorbentassay(ELISA).
RESULTS $---$ Spontaneous IgG production of SLE PBMC was significantly enhanced compared with that found in healthy controls. After PRLstimulation, the IgG concentrations of supernatants from SLE PBMCwere significantly higher than those of unstimulated PBMC (median394 ng/ml). Of note, the physiological concentration of PRL (20ng/ml) induced IgG production more effectively (median 1139 ng/ml)than PRL at 100 ng/ml (median 1029 ng/ml). In contrast, preincubationwith PRL did not stimulate IgG production in normal PBMC. A significantcorrelation between PRL induced IgG production and the diseaseactivity (ECLAM) of the patients with SLE was seen. Moreover,the maximum amount of PRL induced IgG depended on the serum PRLconcentrations of the patients withSLE.
CONCLUSIONS $---$ The results suggest that PBMC from patients with SLE have an extraordinarily high susceptibility to PRL, showing the moststriking effect at a concentration usually found in vivo. Thisindicates a potential role for mild hyperprolactinaemia in thepathogenesis of SLE, influencing both IgG production and diseaseactivity.

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Cohen-Solal, J., Jeganathan, V, Hill, L, Kawabata, D, Pinto-Rodriguez, D, Grimaldi, C, Diamond, B (2008). Hormonal regulation of B-cell function and systemic lupus erythematosus. Lupus 17: 528-532 [Abstract]
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