Opposing roles for TGF-β1 and TGFβ3 isoforms in experimental autoimmune encephalomyelitis

Agata Matejuk, Jami Dwyer, Corwyn Hopke, Arthur A. Vandenbark, Halina Offner

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Hormones can exert significant protective effects on autoimmune diseases by activating immunoregulatory mechanisms. One of the possible mechanisms of hormonal protection might be through the anti-inflammatory effects of the TGF-beta molecule. The present study investigated the changes in expression of two TGF-beta isoforms, TGF-β1 and TGF-β3, in C57BL/6 and TCR transgenic (T/R+) B10.PL mice that manifested or were protected against clinical signs of experimental autoimmune encephalomyelitis (EAE) with 17β-estradiol (E2) treatment. We here demonstrate an inverse relationship between expression of TGF-β1 that is enhanced in mice with EAE, and TGF-β3 that is enhanced in E2-protected mice. The differential expression of TGF-β isoforms was observed in spinal cord tissue but not spleen. Additionally TGF-β1 expression was evident both in whole spinal cord tissue and mononuclear cells isolated from inflamed tissue, in contrast to TGF-β3 that was only detected in spinal cord tissue but not in mononuclear cells. Further studies revealed that CD3 and especially MAC-1 positive cells were the main source of TGF-β1 in the mononuclear CNS population. Of crucial importance, the TGF-β3 isoform displayed anti-proliferative properties towards encephalitogenic cells in vitro. We propose that the TGF-β1 and TGF-β3 isoforms play opposing roles in the expression of EAE.

Original languageEnglish (US)
Pages (from-to)45-51
Number of pages7
Issue number2
StatePublished - Jan 21 2004


  • EAE
  • Estrogen
  • TGF-β1
  • TGF-β3

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology


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