Mechanism and role of phagocytosis of dying cells and microbes

1) sr - bi介导睾丸Sertoli细胞凋亡的机制及作用。睾丸体细胞支持细胞吞噬凋亡的生精细胞后，产生未知因子，使生精细胞向精子分化。为了鉴定该因子，我们通过对支持细胞的蛋白质组学分析选择了一个候选蛋白，并鉴定了其初级结构。我们发现，在吞噬过程中，该因子的表达在转录水平上受到刺激。我们已经培育了该因子的敲除小鼠，我们将在小鼠体内研究该因子在精子发生中的作用。2) TLR-JNK通路在巨噬细胞细菌存活中的作用金黄色葡萄球菌诱导小鼠腹腔巨噬细胞JNK磷酸化依赖toll样受体TLR2。INK通路的激活导致巨噬细胞中超氧化物的产生受到抑制，这使得被吞噬的金黄色葡萄球菌能够在巨噬细胞中存活。流感病毒感染细胞产生巨噬细胞活化因子，通过病毒感染和细胞凋亡两种途径增强病毒感染细胞的巨噬细胞吞噬作用。该因子在热处理后失去了活性，是热不稳定材料。

1) Mechanism and role of SR-BI-mediated apoptotic spermatogenic cells by Sertoli cells in the testis. After phagocytosis of apoptotic spermatogenic cells, testicular somatic Sertoli cells produced unknown factor(s) by which spermatogenic cells could differentiate into spermatozoa. To identify the factor, we selected one candidate protein by proteome analysis of Sertoli cells and identified its primary structure. We found that the expression of the factor was stimulated in transcriptional level during phagocytosis. We have been generating knockout mice of the factor, and we are going to examine the role of the factor on spermatogenesis in mice.2) Role of TLR-JNK pathway on bacterial survival in macrophages Staphylococcus aureus induced JNK phosphorylation in mouse peritoneal macrophages depending on toll-like receptor TLR2. This activation of INK pathway caused inhibition of superoxide production in the macrophages, and this allowed engulfed S. aureus to survive in the macrophages.3) Role of phagocytosis of influenza virus-infected cells by macrophages Influenza virus-infected cells produced macrophage-activating factor that enhance macrophage phagocytosis of virus-infected cells depending on both virus infection and apoptosis. This factor would be heat-labile material since it lost the activity after heat-treatment.