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Regulation of an autoimmune model for multiple sclerosis in Th2-biased GATA3 transgenic mice

International Journal of Molecular Sciences, ISSN: 1422-0067, Vol: 15, Issue: 2, Page: 1700-1718
2014
  • 45
    Citations
  • 0
    Usage
  • 36
    Captures
  • 0
    Mentions
  • 39
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    45
  • Captures
    36
  • Social Media
    39
    • Shares, Likes & Comments
      39
      • Facebook
        39

Article Description

T helper (Th)2 cells have been proposed to play a neuroprotective role in multiple sclerosis (MS). This is mainly based on "loss-of-function" studies in an animal model for MS, experimental autoimmune encephalomyelitis (EAE), using blocking antibodies against Th2 related cytokines, and knockout mice lacking Th2-related molecules. We tested whether an increase of Th2 responses ("gain-of-function" approach) could alter EAE, the approach of novel GATA binding protein 3 (GATA3)-transgenic (tg) mice that overexpress GATA3, a transcription factor required for Th2 differentiation. In EAE induced with myelin oligodendrocyte glycoprotein (MOG) peptide, GATA3-tg mice had a significantly delayed onset of disease and a less severe maximum clinical score, compared with wild-type C57BL/6 mice. Histologically, GATA3-tg mice had decreased levels of meningitis and demyelination in the spinal cord, and anti-inflammatory cytokine profiles immunologically, however both groups developed similar levels of MOG-specific lymphoproliferative responses. During the early stage, we detected higher levels of interleukin (IL)-4 and IL-10, with MOG and mitogen stimulation of regional lymph node cells in GATA3-tg mice. During the late stage, only mitogen stimulation induced higher IL-4 and lower interferon-γ and IL-17 production in GATA3-tg mice. These results suggest that a preexisting bias toward a Th2 immune response may reduce the severity of inflammatory demyelinating diseases, including MS. © 2014 by the authors; licensee MDPI, Basel, Switzerland.

Bibliographic Details

Fernando, Viromi; Omura, Seiichi; Sato, Fumitaka; Kawai, Eiichiro; Martinez, Nicholas E; Elliott, Sadie Faith; Yoh, Keigyou; Takahashi, Satoru; Tsunoda, Ikuo

MDPI AG

Chemical Engineering; Biochemistry, Genetics and Molecular Biology; Chemistry; Computer Science

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