C1q and mannose binding lectin engagement of cell surface calreticulin and CD91 initiates macropinocytosis and uptake of apoptotic cells.
C1q and mannose binding lectin engagement of cell surface calreticulin and CD91 initiates macropinocytosis and uptake of apoptotic cells.
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DOI：
10.1084/jem.194.6.781
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发表时间：
2001-09-17
期刊：
影响因子：
--
通讯作者：
Henson PM
中科院分区：
文献类型：
--
作者：
Ogden CA;deCathelineau A;Hoffmann PR;Bratton D;Ghebrehiwet B;Fadok VA;Henson PM
去除凋亡细胞对于维持组织稳态、器官发生、重塑、发育和免疫系统的维持、防止肿瘤形成和消除炎症至关重要。这种去除的机制涉及凋亡细胞表面的识别和多种细胞类型的吞噬细胞的摄取的启动。在这里，我们提供的证据表明，C1q 和甘露糖结合凝集素 (MBL)（蛋白质集合素家族的成员）与凋亡细胞结合，并通过连接多功能蛋白质钙网蛋白（也称为 cC1qR）的吞噬细胞表面来刺激这些细胞的摄取，而钙网蛋白又与内吞受体蛋白 CD91（也称为 α-2-巨球蛋白受体）结合。这些蛋白质的使用提供了先天免疫系统的模式识别分子介导的凋亡细胞清除的另一个例子。通过钙网蛋白/CD91刺激摄取凋亡细胞被进一步证明涉及巨胞饮作用过程，这表明C1q和MBL增强吞噬整个、完整的凋亡细胞以及这些分子可能结合的细胞碎片和外来生物体的原始且相对非选择性的摄取机制。
Removal of apoptotic cells is essential for maintenance of tissue homeostasis, organogenesis, remodeling, development, and maintenance of the immune system, protection against neoplasia, and resolution of inflammation. The mechanisms of this removal involve recognition of the apoptotic cell surface and initiation of phagocytic uptake into a variety of cell types. Here we provide evidence that C1q and mannose binding lectin (MBL), a member of the collectin family of proteins, bind to apoptotic cells and stimulate ingestion of these by ligation on the phagocyte surface of the multifunctional protein, calreticulin (also known as the cC1qR), which in turn is bound to the endocytic receptor protein CD91, also known as the α-2-macroglobulin receptor. Use of these proteins provides another example of apoptotic cell clearance mediated by pattern recognition molecules of the innate immune system. Ingestion of the apoptotic cells through calreticulin/CD91 stimulation is further shown to involve the process of macropinocytosis, implicated as a primitive and relatively nonselective uptake mechanism for C1q- and MBL-enhanced engulfment of whole, intact apoptotic cells, as well as cell debris and foreign organisms to which these molecules may bind.
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影响因子：
32.4
作者：
Basu, S;Binder, RJ;Srivastava, PK
通讯作者：
Srivastava, PK
影响因子：
--
作者：
DAVIES, EJ;SNOWDEN, N;OLLIER, WER
通讯作者：
OLLIER, WER
影响因子：
30.5
作者：
Binder, RJ;Han, DK;Srivastava, PK
通讯作者：
Srivastava, PK
影响因子：
3.5
作者：
D'Cruz, PM;Yasumura, D;Vollrath, D
通讯作者：
Vollrath, D
影响因子：
3.4
作者：
Bronson, R;Bronson, S;Ghebrehiwet, B
通讯作者：
Ghebrehiwet, B