SEPARATION OF SELF FROM NON-SELF IN THE COMPLEMENT-SYSTEM
SEPARATION OF SELF FROM NON-SELF IN THE COMPLEMENT-SYSTEM
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DOI：
10.1016/0167-5699(87)90167-8
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发表时间：
1987-07-01
期刊：
影响因子：
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通讯作者：
FARRIES, T
中科院分区：
文献类型：
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作者：
ATKINSON, JP;FARRIES, T
替代补体途径是一种自我包含且独立的识别和效应途径，其进化目的是保护宿主免受微生物侵害。因此，它必须将自我与非自我分开（通过关键 C3 组件的低级连续周转（fickover）），a/temat/ve 补体途径始终保持警惕以保护宿主。活化的 C3 持续与自身组织和外来组织（如果存在）结合。在此启动步骤中不存在明显的歧视。然而，C3 在自身（而非外来）组织上沉积的放大（这是建立该途径的效应子功能的必要条件）受到一系列功能、结构和遗传相关的血浆和膜糖蛋白的抑制，这些糖蛋白下调补体激活。这些调节分子广泛分布在人体组织上。血浆蛋白优先对液相成分起作用，膜结合形式作用于细胞结合成分。在此，约翰·阿特金森 (John Atkinson) 和蒂莫西·法里斯 (Timothy Farries) 讨论了这些补体激活抑制剂，并提出它们的作用说明了 Lhe a! 的能力！ termtive n,= th~-~ u tn............ i,,,~,, vv~ l,, v 在外源 P= sue 上扩增，但在自体组织上下调。传统上，补体系统被认为代表体液免疫系统的效应臂。在免疫宿主中，抗体选择靶标，产生的抗原-抗体复合物可能激活经典的补体途径。该途径通过将其调理性（C3b、C4b）片段沉积在被人类免疫系统识别为外源的抗原上，帮助抗体处理免疫复合物。这些结合的调理子片段反过来可以与补体受体相互作用，并且 C3b 也可以启动末端裂解复合物。趋化因子和过敏毒素的释放促进炎症反应。从这个角度来看！替代途径只是在免疫复合物形成并固定补体的位点放大 C3 沉积的一种手段。看待该系统的第二种方式是，替代途径是原始或原始补体系统，而经典途径主要是一种连接手段；另一种（体液）免疫系统
The alternative complement pathway is a serf-contained and independent recognition and effector pathway that evolved to protect the host from microbes. As such, it must separate self from non-self Via low grade continuous turnover fiickover) of the pivotal C3 component, the a/temat/ve complement pathway is always on guard to defend the host. Activated C3 binds continuously to self tissue and to foreign tissue, if present. There is no apparent discrimination at this initiation step. However, the amplification of C3 deposition on self (but not foreign) tissue, a necessity in establishing the effector fun~'ons of this pathway is inhibited by a series of func~ bnally, structurally and genetically related plasma and membrane glycopro~'ns which down-regulate complement activation. These regulatory molecules are widely distributed on human tissue. The plasma proteins are preferentially active on fluid-phase components~ Vnile membrane-bound forms act on ceil-bound components. Here, John Atkinson and timothy Farries discuss these inhibitors of complement activation and suggest that their action explat'm_ the abih'ty of Lhe a! termtive n,= th~-~ u tn............ i,,,~,, vv~ l,, v amplify on foreign P= sue but be down-regulated on autologous tissue.Traditionally, the complement system has been considered to represent an effector arm of the humoral immune system. In the immune host, antibody selects the target and the resulting antigen-antibody complex may activate the classical complement pathway. This pathway assists antibody in the handling of immune complexes through the deposition of its opsonic (C3b, C4b) fragments on antigens recognized as foreign by the hJmoral immune system. These bound opsonic fragments can in turn interact with complement receptors and C3b can also initiate the terminal lytic complex. The inflammatory response is promoted by the release of chemotactic factors and anaphylatoxins. In this view of comp! ement a.-tivation the alternative pathway is just a means of amplifying C3 deposition at the site where the immune complex has formed and fixed complement. A second way of looking at the system is that the alternative pathway is the primitive or original complement system and the classical pathway is primarily a means of connect; ng another (humoral) immune s~ stem