MOLECULAR MECHANISMS OF MACROPHAGE ACTIVATION BY LPS

我们一直对宿主防御机制感兴趣。 肿瘤细胞。当巨噬细胞被细菌刺激时 脂多糖(LPS)，它们对多种细胞具有高度的细胞毒性 肿瘤细胞。为了了解所涉及的分子机制 在这个过程中，我们计划(L)表征内毒素反应元件 (LRE)在即刻早期基因启动子区域转录 脂多糖激活，(2)鉴定和分离转录因子(S) 与LRE相关的基因和(3)分离称为LPs的基因 控制小鼠和小鼠巨噬细胞对内毒素的反应性。 巨噬细胞对内毒素刺激的反应可以在没有 T或B淋巴细胞的参与，很可能代表了一种 对潜在病原体的原始防御反应。澄清： 这一过程中涉及的分子机制将促进我们的 对内毒素所致感染性休克及抗癌药物作用的认识 紫杉醇，以及对各种潜在的 有害物质，包括病毒和肿瘤细胞。

We have been interested in the mechanisms of host defense against neoplastic cells. When macrophages are stimulated with bacterial lipopolysaccharide (LPS), they become highly cytotoxic to a variety of neoplastic cells. In order to understand the molecular mechanisms involved in this process, we plan to (l) characterize the LPS-responsive elements (LRE) in promoter regions of the immediate early genes transcriptionally activated by LPS, (2) characterize and isolate transcription factor(s) that become associated with LRE and (3) isolate the gene called lps that controls the responsiveness of mouse and murine macrophages to LPS. The responses of macrophages to LPS stimulation can occur without the participation of T or B lymphocytes, and may very well represent a primitive defense reaction against potential pathogens. Elucidation of molecular mechanisms involved in this process will advance our understanding of septic shock caused by LPS, action of anticancer drug Taxol, as well as natural immunity against a variety of potentially harmful agents including virus and neoplastic cells.