title: Prolactin is not required for the development of severe chronic experimental autoimmune encephalomyelitis.
abstract: Predominance of multiple sclerosis (MS) in women, reductions of disease flares during pregnancy, and their increase in the postpartum period have suggested a hormonal influence on MS activity. The hormone prolactin (PRL) has long been debated as a potential immune-stimulating factor in several autoimmune disorders, including MS and its animal model experimental autoimmune encephalomyelitis (EAE). However, to date, no data clearly ascribe a pathogenic role to PRL in these diseases. Using PRL receptor-deficient (Prlr(-/-)) and PRL-deficient (Prl(-/-)) mice, we show that PRL plays a redundant role in the development of chronic EAE. In Prlr(-/-) and Prl(-/-) mice, EAE developed with a delayed onset compared with littermate control mice, but with full clinical severity. In line with the clinical outcome, T cell proliferation and production of IFN-γ, IL-17A, and IL-6 induced by myelin Ag were delayed in Prlr(-/-) and Prl(-/-) mice. Ag-specific IgG Ab responses were not affected by PRLR or PRL deficiency. We also show that mouse lymph node cells and purified CD4(+) T cells express transcript for Prlr, but not for Prl. These results reveal that PRL does not play a central role in the development of chronic EAE and optimal Th1 and Th17 responses against myelin. Moreover, they also rule out a possible contribution of PRL secreted by immune cells to the modulation of autoreactive T cell response in this model.
authors.affiliation: Neuroimmunology and Neuromuscular Disorder Unit, Foundation IRCCS Neurological Institute Carlo Besta, 20133 Milan, Italy.
authors.forename: Massimo
authors.initials: M
authors.lastname: Costanza
authors.forename: Silvia
authors.initials: S
authors.lastname: Musio
authors.forename: Mhamad
authors.initials: M
authors.lastname: Abou-Hamdan
authors.forename: Nadine
authors.initials: N
authors.lastname: Binart
authors.forename: Rosetta
authors.initials: R
authors.lastname: Pedotti
mesh_terms: D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D011388:Prolactin / Q000276:immunology* / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D011388:Prolactin