MAC-1 AND P150,95 AVIDITY CHANGES IN TRANSFECTED CELLS

中性粒细胞和单核细胞迁移和粘附到炎症组织是 对正常免疫功能至关重要，是早期免疫缺陷的重要组成部分。 肾小球肾炎和急性肾移植排斥反应。 白细胞 整合素，Mac-1和p150，95，是骨髓单核细胞 相互粘附、粘附于内皮细胞和粘附于人肾小球系膜细胞。 这种结合功能受细胞刺激调节， 化学引诱物或佛波醇酯;第二信使参与 仍有待确定。 本项目的目标是研究 或Mac-1和p150，95的亲合力， 表征两种分子的配体的组织分布。 我们将使用的策略是：1）检测人Mac-1和p150，95 转化为小鼠杂交瘤T细胞系（其中一些在第二免疫缺陷中是缺陷的）。 信使产生），2）分析Mac-1和p150.95亲和力的变化， 细胞刺激后转染的细胞，以及3）评估 人中性粒细胞/内皮细胞、细胞基质的转染子 成分和冷冻组织切片。 鼠T细胞杂交瘤的应用 因为转染子将允许分析整合素亲合力的变化， 用抗原进行细胞刺激，以及缺乏 第二信使的产生将使我们能够剖析 整合素结合的变化。 此外，其他方面的互动 通过使用以下物质将避免物种特异性的表面分子： 小鼠T细胞杂交瘤。

Neutrophil and monocyte migration and adherence to inflamed tissue are essential for normal immune function and are important components of early glomerulonephritis and acute renal allograft rejection. The leukocyte integrins, Mac-1 and p150,95, are essential for myelomonocytic cells to adhere to each other, to endothelial cells and to human mesangial cells. This binding function is regulated by cellular stimulation with chemoattractants or by phorbol esters; the second messengers involved remain to be defined. The goals of this project are to study the binding or avidity of Mac-1 and p150,95 after cellular stimulation and to characterize the tissue distribution of the ligands for both molecules. The strategy we will use will be to: 1) transfect human Mac-1 and p150,95 into mouse hybridoma T cell lines (some of which are deficient in second messenger production), 2) analyze changes in Mac-1 and p150.95 avidity in transfected cells after cellular stimulation and, 3) assess the binding of transfectants to human neutrophils/endothelial cells, cell matrix components and frozen tissue sections. The use of murine T cell hybridomas as transfectants will permit an analysis of integrin avidity change after cellular stimulation with antigen, and the use of hybridomas deficient in second messenger production will allow us to dissect the pathways involved in the change in integrin binding. In addition, interactions by other surface molecules that are species specific will be avoided by the use of mouse T-cell hybridomas.