C-Reactive protein binds to apoptotic cells, protects the cells from assembly of the terminal complement components, and sustains an antiinflammatory innate immune response: implications for systemic autoimmunity.
C-Reactive protein binds to apoptotic cells, protects the cells from assembly of the terminal complement components, and sustains an antiinflammatory innate immune response: implications for systemic autoimmunity.
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C反应蛋白与凋亡细胞结合，保护细胞免受末端补体组件的组装，并维持抗炎的先天免疫反应：对系统性自身免疫的影响。
DOI：
10.1084/jem.192.9.1353
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发表时间：
2000-11-06
期刊：
影响因子：
--
通讯作者：
Elkon KB
中科院分区：
文献类型：
--
作者：
Gershov D;Kim S;Brot N;Elkon KB
C-反应蛋白（CRP）是一种血清蛋白，作为对感染和组织损伤的先天免疫应答的一部分被大量诱导。由于CRP已在受损组织中检测到，并且已知可激活补体，因此我们评估了凋亡淋巴细胞是否结合CRP，并确定结合对先天免疫的影响。CRP以Ca 2+依赖的方式与凋亡细胞结合，并增强补体激活的经典途径，但保护细胞免于末端补体成分的组装。此外，CRP增强了巨噬细胞对凋亡细胞的调理作用和吞噬作用，与巨噬细胞因子转化生长因子β的表达相关。CRP的抗肿瘤作用需要C1 q和H因子，一旦细胞坏死就无效。这些观察结果表明，CRP和经典的补体成分一致行动，以促进非炎症清除凋亡细胞，并可能有助于解释如何经典途径和某些pentraxins的缺陷导致受损的处理凋亡细胞和增加坏死的可能性免疫反应自我。
C-reactive protein (CRP) is a serum protein that is massively induced as part of the innate immune response to infection and tissue injury. As CRP has been detected in damaged tissues and is known to activate complement, we assessed whether apoptotic lymphocytes bound CRP and determined the effect of binding on innate immunity. CRP bound to apoptotic cells in a Ca2+-dependent manner and augmented the classical pathway of complement activation but protected the cells from assembly of the terminal complement components. Furthermore, CRP enhanced opsonization and phagocytosis of apoptotic cells by macrophages associated with the expression of the antiinflammatory cytokine transforming growth factor β. The antiinflammatory effects of CRP required C1q and factor H and were not effective once cells had become necrotic. These observations demonstrate that CRP and the classical complement components act in concert to promote noninflammatory clearance of apoptotic cells and may help to explain how deficiencies of the classical pathway and certain pentraxins lead to impaired handling of apoptotic cells and increased necrosis with the likelihood of immune response to self.
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影响因子：
15.9
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM
DOI：
10.1016/s0167-5699(97)01002-5
发表时间：
1997-03-01
期刊：
IMMUNOLOGY TODAY
影响因子：
--
作者：
Hack, CE;Wolbink, GJ;vandenBosch, H
通讯作者：
vandenBosch, H
DOI：
10.1084/jem.190.12.1733
发表时间：
1999-12-20
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Griselli M;Herbert J;Hutchinson WL;Taylor KM;Sohail M;Krausz T;Pepys MB
通讯作者：
Pepys MB
影响因子：
15.9
作者：
FIRESTEIN, GS;YEO, M;ZVAIFLER, NJ
通讯作者：
ZVAIFLER, NJ
影响因子：
15.3
作者：
KUSHNER, I;KAPLAN, MH
通讯作者：
KAPLAN, MH