Abstract
To analyze the role of the Th2 cytokine interleukin-5 (IL-5) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-5 gene-knockout (KO) mice in the C57BL/6 background. IL-5 KO mice had a significantly reduced incidence and severity of EAMG. Despite their increased resistance to EAMG, IL-5 KO mice displayed intact secondary antibody and lymphoproliferative responses to acetylcholine receptor (AChR) after immunization with this molecule. However, the relative resistance of IL-5 KO mice was associated with a reduced primary lymphocyte response to AChR, and reduced C3 levels in muscle extracts compared to those in C57BL/6 mice.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 51-58 |
| Number of pages | 8 |
| Journal | Journal of Neuroimmunology |
| Volume | 125 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - 2002 |
| Externally published | Yes |
Keywords
- Autoimmunity
- IL-5
- IL-5 gene knockout
- Immunomodulation
- Myasthenia gravis
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology