Abstract
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 language | English (US) |
|---|---|
| Pages (from-to) | 45-51 |
| Number of pages | 7 |
| Journal | Cytokine |
| Volume | 25 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 21 2004 |
Keywords
- EAE
- Estrogen
- TGF-β1
- TGF-β3
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Biochemistry
- Hematology
- Molecular Biology