ROLE OF SCAVENGER RECEPTORS IN MACROPHAGE ACTIVATION AND THEIR APPLICATION FOR DIAGNOSIS AND THERAPY

利用A类清道夫受体（SR-A, CD204）缺失的巨噬细胞，我们发现SR-A通过竞争性地抑制LPS与TLR4的结合来抑制巨噬细胞的激活。结果表明SR-A在lps诱导的炎症反应调控中起关键作用。肿瘤中cd163阳性巨噬细胞密度与胶质瘤和上皮性卵巢癌的恶性分级呈正相关。我们发现M2巨噬细胞与肿瘤细胞通过STAT3相互作用。通过筛选天然化合物，发现柯罗果酸对巨噬细胞的M2极化有抑制作用。这种化合物可能成为预防和治疗肿瘤的潜在新工具。

Using class A scavenger receptor (SR-A, CD204)-deficient macrophages, we disclosed that SR-A suppresses the macrophage activation by inhibiting the binding of LPS to TLR4 in a competitive manner. The result indicates SR-A plays a pivotal role in the regulation of the LPS-induced inflammatory response. Density of CD163-positive macrophages in tumors positively correlated with the malignant grade of glioma and epithelial ovarian cancer. It was found that M2 macrophages and tumor cells interact via STAT3. By screening natural compounds, corosolic acid was found to suppress M2 polarization of macrophages. This compound could be a potentially new tool for tumor prevention and therapy.