## Abstract A mouse model of MG, termed experimental autoimmune myasthenia gravis (EAMG), can be obtained after immunization with __Torpedo__ acetylcholine receptor (AChR). Although many studies have detailed the consequence of AChR antibodies binding at the neuromuscular junction and the difficult
Macrophage apoptosis in muscle tissue in experimental autoimmune myasthenia gravis
β Scribed by Fu-Dong Shi; Xue-Feng Bai; Hu-Lun Li; Hans Link
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 237 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0148-639X
No coin nor oath required. For personal study only.
β¦ Synopsis
Combining in situ tailing and immunocytochemical staining, we demonstrated that the infiltrating macrophages in muscle tissue sections during early phase of experimental autoimmune myasthenia gravis (EAMG) in Lewis rats were eliminated by apoptosis at high frequency. These apoptotic macrophages were colocalized in the end-plate regions. Apoptosis is a major cause for elimination of infiltrating macrophages during the early phase of EAMG.
π SIMILAR VOLUMES
## Abstract Use of the mouse model of myasthenia gravis (murine EAMG), ideally suited for immunological study, has been hampered by the relatively mild character of the disease and by the extended time and effort required for inducing severe disease. Electromyographic measurement of the compound ac
## Abstract Immunization of groups of rats with 0.1β100 ΞΌg of acetylcholine receptor (AChR) purified from the electric organ of __Torpedo californica__ resulted in doseβdependent (1) loss of acetylcholine receptor from the rats' muscles, (2) binding of antibodies to many of the receptors remaining