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Int. J. Mol. Sci. 2016, 17(12), 2026; doi:10.3390/ijms17122026

Prolactin: Friend or Foe in Central Nervous System Autoimmune Inflammation?

Department of Clinical Neuroscience, Neurological Institute Foundation IRCCS Carlo Besta, 20133 Milan, Italy
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Authors to whom correspondence should be addressed.
Academic Editors: Christoph Kleinschnitz, Sven Meuth and Irmgard Tegeder
Received: 9 October 2016 / Revised: 19 November 2016 / Accepted: 28 November 2016 / Published: 2 December 2016
(This article belongs to the Special Issue Advances in Multiple Sclerosis 2016)
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Abstract

The higher prevalence of multiple sclerosis (MS) in females, along with the modulation of disease activity observed during pregnancy and the post-partum period, has suggested a hormonal influence in MS. Even if prolactin (PRL) does not belong to the sex hormones family, its crucial role in female reproduction and lactation has prompted great efforts to understand if PRL could represent a gender factor in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), the animal model for this disease. Extensive literature has documented a remarkable immune-stimulating potential for this hormone, indicating PRL as a disease-promoting factor in MS and EAE. However, recent work has pointed out that PRL is endowed with important neuroprotective and remyelinating properties and has encouraged a reinterpretation of the involvement of this hormone in MS. In this review we summarize both the protective functions that PRL exerts in central nervous system tissue as well as the inflammatory activity of this hormone in the context of autoimmune responses against myelin. Last, we draw future lines of research that might help to better clarify the impact of PRL on MS pathology. View Full-Text
Keywords: prolactin; multiple sclerosis; experimental autoimmune encephalomyelitis; neuroinflammation; neuroprotection prolactin; multiple sclerosis; experimental autoimmune encephalomyelitis; neuroinflammation; neuroprotection
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Costanza, M.; Pedotti, R. Prolactin: Friend or Foe in Central Nervous System Autoimmune Inflammation? Int. J. Mol. Sci. 2016, 17, 2026.

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