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 journalArticle

15 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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