Streptococcus pneumoniae interactions with the complement system.
Streptococcus pneumoniae interactions with the complement system.
复制标题
肺炎链球菌与补体系统的相互作用。
DOI：
10.3389/fcimb.2022.929483
复制
发表时间：
2022
影响因子：
5.7
通讯作者：
Brown, Jeremy S.
中科院分区：
文献类型：
--
作者：
Gil, Eliza;Noursadeghi, Mahdad;Brown, Jeremy S.
关键词：
宿主对肺炎链球菌感染的固有免疫和适应性免疫严重依赖补体系统，这一点通过补体成分遗传性缺陷患者中侵袭性肺炎链球菌感染的高发病率得以证明。补体系统通过多种机制被肺炎链球菌激活。经典补体途径通过C - 反应蛋白、血清淀粉样蛋白P、C1q、SIGN - R1或天然或获得性抗体对肺炎链球菌的识别而被激活。一些肺炎链球菌菌株也可被纤维胶凝蛋白识别，从而激活甘露糖结合凝集素（MBL）激活途径。然后，替代补体途径会放大补体激活，而替代补体途径也可被肺炎链球菌直接激活。补体激活导致调理补体因子C3b和iC3b与肺炎链球菌表面共价连接，这促进了吞噬清除，以及补体介导的对红细胞的免疫黏附，从而预防败血症。补体在肺炎链球菌黏膜免疫中的作用不太明确。鉴于补体在控制肺炎链球菌感染中起主要作用，肺炎链球菌进化出多种逃避补体的机制也就不足为奇了，这些机制包括荚膜、多种表面蛋白以及毒素肺炎溶素。肺炎链球菌荚膜血清型和基因型在对补体的敏感性方面存在相当大的差异，这与引起侵袭性感染的能力相关。然而，目前我们对导致肺炎链球菌菌株之间以及与非致病性链球菌之间补体敏感性差异的主要机制了解有限。
Host innate and adaptive immunity to infection with Streptococcus pneumoniae is critically dependent on the complement system, demonstrated by the high incidence of invasive S. pneumoniae infection in people with inherited deficiency of complement components. The complement system is activated by S. pneumoniae through multiple mechanisms. The classical complement pathway is activated by recognition of S. pneumoniae by C-reactive protein, serum amyloid P, C1q, SIGN-R1, or natural or acquired antibody. Some S. pneumoniae strains are also recognised by ficolins to activate the mannose binding lectin (MBL) activation pathway. Complement activation is then amplified by the alternative complement pathway, which can also be activated by S. pneumoniae directly. Complement activation results in covalent linkage of the opsonic complement factors C3b and iC3b to the S. pneumoniae surface which promote phagocytic clearance, along with complement-mediated immune adherence to erythrocytes, thereby protecting against septicaemia. The role of complement for mucosal immunity to S. pneumoniae is less clear. Given the major role of complement in controlling infection with S. pneumoniae, it is perhaps unsurprising that S. pneumoniae has evolved multiple mechanisms of complement evasion, including the capsule, multiple surface proteins, and the toxin pneumolysin. There is considerable variation between S. pneumoniae capsular serotypes and genotypes with regards to sensitivity to complement which correlates with ability to cause invasive infections. However, at present we only have a limited understanding of the main mechanisms causing variations in complement sensitivity between S. pneumoniae strains and to non-pathogenic streptococci.
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DOI：
10.1084/jem.20161621
发表时间：
2017-05-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Deniset JF;Surewaard BG;Lee WY;Kubes P
通讯作者：
Kubes P
影响因子：
3.1
作者：
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通讯作者：
Malley, Richard
影响因子：
30.3
作者：
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通讯作者：
Weiser JN
影响因子：
30.3
作者：
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通讯作者：
Verschoor, Admar
DOI：
10.2174/187153008786848321
发表时间：
2008-12
期刊：
Endocrine, metabolic & immune disorders drug targets
影响因子：
--
作者：
Agrawal A;Suresh MV;Singh SK;Ferguson DA Jr
通讯作者：
Ferguson DA Jr