Prolactin: Friend or foe in central nervous system autoimmune inflammation?

Massimo Costanza, Rosetta Pedotti

Research output: Contribution to journalReview article

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.

Original languageEnglish
Article number2026
JournalInternational Journal of Molecular Sciences
Volume17
Issue number12
DOIs
Publication statusPublished - Dec 2 2016

Keywords

  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis
  • Neuroinflammation
  • Neuroprotection
  • Prolactin

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Computer Science Applications
  • Spectroscopy
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Fingerprint Dive into the research topics of 'Prolactin: Friend or foe in central nervous system autoimmune inflammation?'. Together they form a unique fingerprint.

  • Cite this