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【单句求助】Chapter 2 Innate Immunity：The First Lines of Defence 50—51页的翻译

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The proteins of the alternative pathway were discovered later and are designated by different capital letters, for example
factorB and factor D.
随后发现了旁路蛋白，并以不同的大写字母命名，如B因子和C因子。
（旁路：补体成分C3、C5到C9在没有C1、C2和**参加时被激活的途径。又称裂解素途径。例如它可被人IgA激活）
Their cleavage products are also designated by the addition of lower-case a and b: thus, the large fragment of B is called Bb and the small fragment Ba.
它们的分解产物也以小写字母a和b命名，因而，B裂解产生的较大的那个片段被称为Bb,而小点的那个片段叫Ba。
Activated complement components are sometimes designated by a horizontal line, for example,C2a; however, we will not use this convention. All thecomponentsof the complement system are listed in Fig. 2.11.
激活的补体成分有时在命名时会加一横线，如，C2a-；然而，我们并不使用这一惯例。所有补体系统的成分都列举在表2.11中。
Besides acting in innate immunity, complement also influences adaptive immunity.
除了在天然免疫中起作用，补体也影响获得性免疫。
Opsonization of pathogens by complement facilitates their uptake by phagocytic antigen-presenting cells that express complement receptors; this enhances the presentation of pathogen antigens to T cells, which we discuss in more detail in Chapter 6.
病原体通过补体产生的调理素作用促使自身被吞噬细胞的抗原提呈细胞摄取，这些抗原提呈细胞表达补体受体；这可加强病原体对T细胞的抗原表达，我们将在第六章中详细阐述。
B cells express receptors for complement proteins that enhance their responses to complement-coated antigens, as we describe later in Chapter 10.
B细胞表达补体蛋白的受体，这些补体蛋白可以加强B细胞对补体覆盖的抗原的反应，我们随后将在第10章中阐述。
In addition, several of thecomplement fragments canact to influence cytokine production by antigen-presenting cells, thereby influencing the direction and extent of the subsequent adaptive immuneresponse, as we describe in Chapter 11.
此外，一些补体片段能影响抗原提呈细胞产生细胞因子，从而影响获得性免疫反应的方向和程度，我们在第11章中进行了描述。
2-5 The complement system recognizes features ofmicrobial surfaces and marks them for destruction by the deposition of C3b.
2-5补体系统可辨识微生物表面的特点并进行标记以便通过C3b的沉积进行破坏
Figure 2.12 gives a highly simplified preview of the initiation mechanisms andoutcomes of complement activation.
表2.12给出了一个高度精炼的关于补体激活的启动机制和结果的预览。
Thethree pathways of complement activation are initiated in different ways.
补体激活的三个通道通过不同的方式启动
The lectin pathway is initiated by soluble carbohydrate-binding proteins-mannose-binding lectin and the ficolins-that bind to particular carbohydrate structures on microbial surfaces.
可溶的碳水化合物结合到蛋白-甘露糖，结合到凝集素和微生物表面的特定碳水化合物结构结合的ficolins，启动了凝集素通路
Proteases associated with these recognition proteins then trigger the cleavage ofcomplement proteins and activation of the pathway.
与这些识别蛋白相关的蛋白酶会触发补体蛋白的裂解和通路的激活。
Theclassical pathway is initiated when the complement component C1, whichcomprises a recognition protein (C1q) associated with proteases (C1r and C1s), either recognizes a microbial surfacedirectly or binds to antibodies already bound to a pathogen.
补体成分C1 包含了识别蛋白C1q，与蛋白酶（C1r和C1s）结合在一起, 当C1直接识别微生物表面或者与抗原上结合的抗体结合，均能启动经典通路。
Finally, the alternative pathway can beinitiated by spontaneous hydrolysis and activation of the complementcomponent C3, which can then bind directly to microbial surfaces.
最后，补体成分C3的自发水解和激活可以激活旁路，C3直接与微生物表面结合。
These three pathways converge at the central and most important step in complement activation. When any of the pathways interacts with apathogen surface, an enzymatic activity called a C3 convertase is generated.
这三个通路会聚在补体激活的最中心和最重要的一步。当任何一个通路与病原体与病原体表面相互作用时，会产生酶活性（？），被称为C3转化酶。
There are various types of C3 convertase, depending on thecomplement pathway activated, but each is a multisubunit protein with protease activity that cleaves complement component 3 (C3).
C3转化酶有多种形式，这取决于激活的补体通路，每种都是具有裂解C3补体的蛋白酶活性的多个亚基组成的蛋白。
The C3 convertase is bound covalently to
the pathogen surface, where it cleavesC3 to generate large amounts of C3b, the main effector molecule of the complement system, and C3a, a peptide that helps induce inflammation.
C3转化酶与病原体表面共价结合，如果裂解了C3产生大量的C3b，补体系统主要的效应分子，和C3a，有助于诱导炎性反应的多肽。
Cleavage of C3 is the critical step in complement activation and leads directly or indirectly to all theeffector activities of
the complement system (see Fig. 2.12).
C3的裂解是补体激活的关键步骤，并且会直接导致或间接引起补体系统所有的效应产物激活（见表2.12）。
C3b binds covalently to the microbial surface and acts as an opsonin, enabling phagocytes that carry receptors for complement to take up and destroy the C3b-coated microbe.
C3b与微生物表面共价结合，C3b作为调理素，使具有补体受体的吞噬细胞摄取并且破坏C3b覆盖的微生物。
We describe the different complement receptors involved in this function of the complement system later in thechapter.
我们将在后面的章节叙述补体系统的这个功能相关的各个补体受体。
C3b can also bind to the C3 convertases formed by the classical and lectin pathways,forming another multisubunit enzyme, a C5 convertase (not shown in Fig. 2.12).
C3b能与经典路径和凝集素路径形成的C3转化酶结合，形成另一种多个亚基构成的酶，一种C5转化酶（表2.12中未列出）
This cleaves C5, liberating the highly inflammatory peptide C5a and generating C5b.
这种酶可以分解C5，产生炎性肽类（？）C5a，还有C5b。
C5b initiates the 'late' events of complement activation, in which a further set of complement proteins interact with C5b to form amembrane-attack complex on the pathogen surface, creating a pore in the cell membrane that leads to cell lysis.
C5b启动了补体激活的晚期事件，在这个事件当中，一系列的补体蛋白和C5b相互作用在病原体表面形成了膜攻击复合物，在细胞膜上形成了能导致细胞溶解的孔。
Thekey feature of C3b is its ability to form a covalent bond withmicrobial surfaces, which allows the innate recognition of microbes to be translated into effector responses.
C3b的关键特性是它能与微生物表面共价结合，从而使微生物被先天识别（？）这一步能够转换成效应器反应。
Covalent bond formation is due to a highly reactive thioesterbond that is hidden inside the folded C3 protein and cannot react until C3 is cleaved.
共价键形成要归功于隐藏在折叠的C3蛋白中的一个有高度活性的硫酯键，这个硫酯键不能发生反应，除非C3分解。

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兔爷编辑于 2013-08-12 22:03

• 丁香热议——三甲医院被收购后“内斗不休”，院长自杀！

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表2.11
Functionalprotein classes In the complement system
补体系统中功能蛋白的分类
C1q
Binding to antigen:antibody complexes and pathogen surfaces
结合到抗原：抗体复合物和病原体表面
MBL； Ficolins； C1q； Properdin （factor P）
Binding to carbohydrate MBL structures such as Ficolins mannose or GlcNAc on microbial surfaces
结合到碳水化合物MBL结构如Ficolins甘露糖，或
微生物表面的乙酰氨基葡糖
C1r；C1s； C2a； Bb； D； MASP-2
Activating enzymes
激活酶
**b；C3b
Membrane-bindingproteins and opsonins
膜结合的蛋白和调理素
（
调理素：①能使细菌和其他细胞对吞噬作用敏感的一种抗体；②一种非抗体物质，可能是来自补体C3部分，能使细菌对吞噬作用敏感。
）
C5a； C3a；**a
Peptidemediators of inflammation
炎症的多肽类介质
C5b； C6； C7； C8; C9
Membrane-attack proteins
膜攻击蛋白
CR1; CR2;CR3; CR4; CRIg
Complement receptors
补体受体
D1INH;**BP;CR1; MCP; DAF; H; I; P; CD59
Complement-regulatory proteins
补体调节蛋白

2013-08-10 00:23