Clementi F, Sher E
Eur J Cell Biol. 1985 May;37:220-8.
The loss from the cell surface of cholinergic nicotinic receptors induced by exposure to antireceptor antibodies, and the mechanism of this loss has been studied in the BC3H-1 cell line. The maximal effect, i.e. 50% loss of receptors, was observed after 30 min. Receptor loss was due to internalization, which was not accompanied by a detectable increase in fluid phase endocytosis nor by changes in the number and distribution of intramembrane particles (IMP) revealed by freeze-fracture of the plasmalemma. The internalization was specific since the concentration of other receptors exposed at the surface of BC3H-1 cells (alpha and beta adrenergic receptors) was not affected by anticholinergic antibodies. It was temperature-dependent, independent of external calcium, but was blocked by trifluoperazine (TFP), a calmodulin antagonist. The rate of antibodies-induced receptor internalization was much more rapid than that of degradation and furthermore low concentrations of antibodies increased receptor internalization but did not increase receptor degradation. Our findings may be relevant to the clarification of the mechanism of Ab-induced alteration in autoimmune diseases, and in particular in myasthenia gravis.
抗受体抗体暴露诱导胆碱能烟碱样受体从细胞表面丢失，其丢失机制已在BC3H-1细胞系中进行了研究。30分钟后观察到最大效应，即受体丢失50%。受体丢失是由于内化作用，这并未伴随着液相内吞作用的可检测增加，也未伴随着通过质膜冷冻断裂显示的膜内颗粒（IMP）数量和分布的变化。这种内化作用具有特异性，因为暴露于BC3H-1细胞表面的其他受体（α和β肾上腺素能受体）的浓度不受抗胆碱能抗体的影响。它依赖于温度，不依赖于细胞外钙，但被钙调蛋白拮抗剂三氟拉嗪（TFP）阻断。抗体诱导的受体内化速率比降解速率快得多，此外，低浓度抗体增加受体内化但不增加受体降解。我们的发现可能有助于阐明自身免疫性疾病，特别是重症肌无力中抗体诱导改变的机制。
