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tzkcarlos

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专业: 化学计量学与化学信息学

[求助] 自身免疫学翻译为中文-几段话，Autoimmunity Reviews 13 (2014) 108–113

PLA 2 R1 is a type 1 transmembrane receptor that is expressed by podocytes. Besides a short membrane-spanning intracellular domain, the receptor consists of a long extracellular domain with a cysteine-rich head, a ﬁbronectin type II-like repeat domain and eight repeated carbohydrate-recognition domains [22].
PLA 2 R1 is one of four members of the mannose receptor family [23]. All of them have a conserved domain structure and share common characteristics such as constitutive endocytic recycling at the plasma membrane [24] which may provide a constant source of accessible PLA 2 R1 at the podocyte membrane for immune-complex formation [23]. Further more, the receptors exist in both an extended and a bent conformation conferring distinct ligand binding and oligomerization capacities [25]. Since the anti-PLA 2 R1 autoantibodies in patients with pMN only recognize a conformation-dependent target epitope [21], it is assumed that autoantibody-binding might only occur in one of these two conﬁgurations. Therefore, pMN might represent an autoimmune conformational disease (‘conformeropathy’), such as Goodpasture syndrome [1].
Although the exact mechanisms causing pMN are still under investigation, different studies show a strong relationship between antibody levels to podocytic proteins and disease activity. Since the discovery of anti-PLA 2 R1 autoantibodies by Beck et al. in 2009, there has been strong evidence that they are a key player in the pathogenesis [21]. For example, autoantibodies to PLA 2 R1 can not only be eluted from kidney tissue of pMN patients, but also colocalize with PLA 2 R1 in the glomeruli [21]. Therefore, it is widely accepted that upon binding of circulating autoantibodies to PLA 2 R1 on podocytes, subepithelial deposits are formed in situ, leading to complement activation and a cascade of events subsequent to the nephrotic syndrome (in most of the cases) [37]. Interestingly, autoantibodies to PLA 2 R1 have shown to be mainly of the IgG4 subclass, which is regarded as being unable to activate the complement pathway [38,39]. Nevertheless, since the terminal complement compo-
nent C5b-9 is detectable in glomeruli and urine of pMN patients [40,41], there is strong evidence for the involvement of the complement system. As most patients with MN have low or undetectable levels of C1q, the classical complement pathway can be excluded. Therefore, either the alternative or the lectin pathway seems to be predominantly involved [42]. This hypothesis is supported by the notion, that mannose binding lectin can be detected in glomeruli of MN patients [43].

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1楼 2014-08-25 21:09:59

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ssssllllnnnn

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3楼: Originally posted by tzkcarlos at 2014-08-25 10:21:23
有点机器的痕迹，不大通顺。课题组内刊要用的，求修饰更佳版本

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4楼2014-08-25 23:36:10

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ssssllllnnnn

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翻译EPI: 1690
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RXMCDM: 金币+1, 多谢应助！ 2014-08-26 00:17:29
tzkcarlos(phu_grassman代发): 金币+30, he deserves it. Thanks for your cooperation. 2014-08-26 09:53:38

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