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Mechanism and role of phagocytosis of unwanted cells

吞噬不需要的细胞的机制和作用

基本信息

批准号：
16570112
负责人：
SHIRATSUCHI Akiko
金额：
$ 2.24万
依托单位：
Kanazawa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16570112/
关键词：
phagocytosis innate immuniti phosphatidylserine spermatogenesis influenza virus scavenger receptor insect immunity

项目摘要

1) Mechanism and role of SR-BI-mediated apoptotic spermatogenic cells by Sertoli cells in the testisAfter binding of phosphatidylserine on the surface of apoptotic cells, SR-BI in Sertoli cells induces phhosphorylation of MAP kinase p38 and ERKI/II. In the presence of inhibitors for p38-pathway and ERK-pathway, phagocytosis of apoptotic cells by Sertoli cells was inhibited greatly. These results showed that SR-BI, when it binds to phosphatidylserine, transmits signals to activate MAP kinase pathway, which leads to the induction of the engulfment of phosphatidylserine-exposing apoptotic cells by phagocytic cells.2) Role of phagocytosis of ineluenza virus-infected cells by phagocytesIn the lung of influenza virus-infected mice, virus-infected cells were shown in both neutrophils and alveolar macrophages. Administration of the phagocytosis inhibitors into the lung caused both the lethality in mice and the extent of inflammation in the lung were augmented in those mice. These results suggest that phagocytosis of virus-infected cells helps suppress the progress of influenza in mice.3) Regulation of phagosome-lysosome fusionMAP kinase p38-pathway and ERK-pathway were activated in macrophages after incubation with apoptotic cells, and the activity seemed to be needed to phagosome-lysosome fusion in macrophages.

1)SR-BI介导睾丸Sertoli细胞凋亡的机制及作用支持细胞中SR-BI与凋亡细胞表面的磷脂酰丝氨酸结合后，诱导MAP激酶p38和ERKI/II磷酸化。在p38通路和ERK通路抑制剂的存在下，支持细胞对凋亡细胞的吞噬作用受到明显抑制。这些结果表明，SR-BI与磷脂酰丝氨酸结合后，通过信号传导激活MAP激酶通路，导致吞噬细胞对暴露磷脂酰丝氨酸的凋亡细胞的吞噬作用。2）吞噬细胞对流感病毒感染细胞的吞噬作用在流感病毒感染小鼠的肺中，中性粒细胞和肺泡巨噬细胞均可见病毒感染细胞。将吞噬作用抑制剂施用到肺中引起小鼠的致死性和这些小鼠中肺中炎症的程度增加。3）吞噬体-溶酶体融合的调控与凋亡细胞共孵育后，巨噬细胞内MAP激酶p38通路和ERK通路被激活，这可能是巨噬细胞吞噬体-溶酶体融合所必需的。