Mechanism and role of phagocytosis of unwanted cells

1) SR-BI介导睾丸Sertoli细胞致生精细胞凋亡的机制及作用SR-BI与凋亡细胞表面的磷脂酰丝氨酸结合后，可诱导MAP激酶p38和ERKI/II磷酸化。在p38通路和erk通路抑制剂存在的情况下，Sertoli细胞对凋亡细胞的吞噬作用被明显抑制。这些结果表明，SR-BI与磷脂酰丝氨酸结合后，传递信号激活MAP激酶通路，诱导吞噬细胞吞噬暴露于磷脂酰丝氨酸的凋亡细胞。在流感病毒感染小鼠的肺中，嗜中性粒细胞和肺泡巨噬细胞均表现出病毒感染的细胞。将吞噬抑制剂注射到肺中会导致小鼠的死亡和肺部炎症的程度增加。这些结果表明，吞噬病毒感染的细胞有助于抑制小鼠流感的进展。3)巨噬细胞与凋亡细胞孵育后，吞噬体-溶酶体融合map激酶p38通路和erk通路的调控被激活，巨噬细胞吞噬体-溶酶体融合似乎需要这种活性。

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.