Abstract
Lymphotoxin-α (TNF-β) and TNF receptor p55 gene knockout mice are resistant to the development of antibody and complement mediated experimental autoimmune myasthenia gravis (EAMG), suggesting a possible role of TNF in mediating EAMG. Therefore, we tested the hypothesis that blocking the functional interaction of TNF with their receptors by soluble recombinant human TNFR:Fc would suppress the ongoing clinical EAMG. Recombinant human TNFR:Fc administered daily for 2 weeks to C57BL6 mice with ongoing clinical EAMG significantly improved clinical EAMG when compared with placebo-treated mice. A clinical trial of selected myasthenia gravis patients with recombinant human TNFR:Fc could be attempted.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 186-190 |
| Number of pages | 5 |
| Journal | Journal of Neuroimmunology |
| Volume | 122 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - 2002 |
| Externally published | Yes |
Keywords
- Autoimmunity
- Cytokine
- Myasthenia gravis
- TNF receptor
- Therapy
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology