Markedly enhanced susceptibility to experimental autoimmune myasthenia gravis in the absence of decay-accelerating factor protection
J. Clin. Invest. Feng Lin, et al. 110:1269 doi:10.1172/JCI16086 [
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Figure 2Electron micrographs of diaphragm neuromuscular junctions following injection with McAb-3 mAb. (
a) Junction typical of those observed in
Daf1+/+ animals. It appears completely normal with entirely normal synaptic architecture. ×25,000. (
b) Junction from a
Daf1–/– mouse that was obviously weak, shows reduced synaptic folds and a widened synaptic cleft. ×25,000. (
c) Three neuromuscular junctions from
Daf1–/– mice, all exhibiting simplified junctional folds. ×8,000. The electron-dense material seen in the synaptic clefts of the junctions in
b and
c is likely postsynaptic membrane shed from the muscle by complement-mediated destruction. This material is seen in (
d) at a magnification of ×20,000.
