Ravetch J V, Clynes R A
Laboratory of Molecular Genetics and Immunology, Rockefeller University, New York, NY 10021, USA.
Annu Rev Immunol. 1998;16:421-32. doi: 10.1146/annurev.immunol.16.1.421.
Recent results obtained in mice deficient in either FcRs or complement have revealed distinct functions for these two classes of molecules. While each is capable of interacting with antibodies or immune complexes, the two systems mediate distinct biological effector responses. Complement-deficient mice are unable to mediate innate immune responses to several bacterial pathogens and bacterial toxins, yet respond normally to the presence of cytotoxic antibodies and pathogenic immune complexes. In contrast, FcR-deficient mice display no defects in innate immunity or susceptibility to a variety of pathogens, yet they are unable to mediate inflammatory responses to cytotoxic IgG antibodies or IgG immune complexes, despite the presence of a normal complement system. These results lead to the surprising conclusion that these two systems have evolved distinct functions in host immunity, with complement and its receptors mediating the interaction of natural antibodies (IgM) with pathogens to effect protection, while FcRs couple the interaction of IgG antibodies to effector cells to trigger inflammatory sequelae. These results necessitate a fundamental revision of the role of these antibody-binding systems in the immune response.
最近在缺乏FcR或补体的小鼠中获得的结果揭示了这两类分子的不同功能。虽然它们都能够与抗体或免疫复合物相互作用，但这两个系统介导不同的生物效应反应。补体缺陷小鼠无法介导对几种细菌病原体和细菌毒素的固有免疫反应，但对细胞毒性抗体和致病性免疫复合物的存在反应正常。相比之下，FcR缺陷小鼠在固有免疫或对多种病原体的易感性方面没有缺陷，但尽管存在正常的补体系统，它们却无法介导对细胞毒性IgG抗体或IgG免疫复合物的炎症反应。这些结果得出了一个惊人的结论，即这两个系统在宿主免疫中进化出了不同的功能，补体及其受体介导天然抗体（IgM）与病原体的相互作用以实现保护，而FcR则将IgG抗体与效应细胞的相互作用联系起来以触发炎症后遗症。这些结果需要对这些抗体结合系统在免疫反应中的作用进行根本性的修正。
