Oestrogen modulates experimental autoimmune encephalomyelitis and interleukin-17 production via programmed death 1

Chunhe Wang, Babak Dehghani, Yuexin Li, Laurie J. Kaler, Arthur A. Vandenbark, Halina Offner

Research output: Contribution to journalArticlepeer-review

75 Scopus citations

Abstract

The mechanism by which oestrogens suppress experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, is only partially understood. We here demonstrate that treatment with 17β-oestradiol (E2) in C57BL/6 mice boosted the expression of programmed death 1 (PD-1), a negative regulator of immune responses, in the CD4+ FoxP3+ regulatory T (Treg) cell compartment in a dose-dependent manner that correlated with the efficiency of EAE protection. Administration of E2 at pregnancy levels but not lower concentrations also enhanced the frequency of Treg cells. Additionally, E2 treatment drastically reduced the production of interleukin-17 (IL-17) in the periphery of immunized mice. However, E2 treatment did not protect against EAE or suppress IL-17 production in PD-1 gene-deficient mice. Finally, E2 failed to prevent Treg-deficient mice from developing spontaneous EAE. Taken together, our results suggest that E2-induced protection against EAE is mediated by upregulation of PD-1 expression within the Treg-cell compartment.

Original languageEnglish (US)
Pages (from-to)329-335
Number of pages7
JournalImmunology
Volume126
Issue number3
DOIs
StatePublished - Mar 2009

Keywords

  • Experimental autoimmune encephalomyelitis
  • Interleukin-17
  • Oestrogen
  • Programmed death 1
  • Regulatory T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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