Boltz-Nitulescu G, Förster O
Adv Exp Med Biol. 1979;121(A):157-66. doi: 10.1007/978-1-4684-3593-1_14.
Pronase, trypsin and delta-chymotrypsin deplete rat alveolar peritoneal macrophages of EA (IgG)-binding activity. Trypsin and delta-chymotrypsin show an initially--under certain conditions and lasting--enhancement of receptor activity. Cycloheximide, an inhibitor of protein biosynthesis, accelerated the loss of Fc-receptors and inhibited their reappearance. There are differences between alveolar and peritoneal macrophages in the rate of loss as well as of regeneration of Fc-receptors.
链霉蛋白酶、胰蛋白酶和δ-糜蛋白酶可使大鼠肺泡巨噬细胞和腹腔巨噬细胞丧失与EA(IgG)结合的活性。在某些条件下,胰蛋白酶和δ-糜蛋白酶最初会显示出受体活性的增强,且这种增强会持续存在。蛋白质生物合成抑制剂环己酰亚胺加速了Fc受体的丧失,并抑制其重新出现。肺泡巨噬细胞和腹腔巨噬细胞在Fc受体丧失速率和再生速率方面存在差异。