Lachmann P J
Molecular Immunopathology Unit, MRC Centre, Cambridge, UK.
Immunol Today. 1991 Sep;12(9):312-5. doi: 10.1016/0167-5699(91)90005-E.
Complement activation unleashes powerful effector mechanisms against which host cells are protected by homologous restriction factors. These factors are glycolipid-anchored membrane proteins that either induce C3 convertase dissociation (for example decay-accelerating factor) or prevent the full development of the membrane attack complex (for example homologous restriction factor and CD59). In this article Peter Lachmann explores the biology and biochemistry of these important and intriguing molecules.
补体激活会引发强大的效应机制，而宿主细胞通过同源限制因子来抵御这些机制。这些因子是糖脂锚定的膜蛋白，它们要么诱导C3转化酶解离（例如衰变加速因子），要么阻止膜攻击复合物的完全形成（例如同源限制因子和CD59）。在本文中，彼得·拉赫曼探讨了这些重要且有趣的分子的生物学和生物化学特性。
