Prolactin, systemic lupus erythematosus, and autoreactive B cells: Lessons learnt from murine models

Subhrajit Saha, Arlene Tieng, K. Peter Pepeljugoski, Gisele Zandamn-Goddard, Elena Peeva

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

The predominant prevalence of autoimmune diseases in women of reproductive age has led to the investigation of the effects of sex hormones on immune regulation and in autoimmune diseases, in particular the prototypic systemic autoimmune disease lupus. The female hormone prolactin has receptors beyond the reproductive axis including immune cells, and it is thought to promote autoimmunity in human and murine lupus. Induced hyperprolactinemia in experimental lupus models, regardless of gender, exacerbates disease activity and leads to premature death. Prolactin treatment in mice that are not prone to develop lupus leads to the development of a lupus-like phenotype. Persistent mild-moderate hyperprolactinemia alters the selection of the naïve B cell repertoire. Recent studies demonstrate that prolactin impairs all three mechanisms of B cell tolerance induction (negative selection, receptor editing, and anergy) and thereby contributes to the pathogenesis of autoimmunity. The effects of prolactin are genetically determined as shown by the differential response to the hormone in the different mice strains. Bromocriptine, a drug that inhibits prolactin secretion, abrogates some of the immune effects of this hormone. Further research is required to elucidate molecular mechanisms involved in immune effects of prolactin and to develop novel targeted treatments for SLE patients with prolactin-responsive disease.

Original languageEnglish (US)
Pages (from-to)8-15
Number of pages8
JournalClinical Reviews in Allergy and Immunology
Volume40
Issue number1
DOIs
StatePublished - Feb 1 2011

Keywords

  • Autoreactivity B cell tolerance
  • B cell subsets
  • Murine lupus models
  • Prolactin

ASJC Scopus subject areas

  • Immunology and Allergy

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