ANAPHYLATOXIN-MEDIATED REGULATION OF THE IMMUNE RESPONSE

过敏毒素介导的免疫反应调节

基本信息

批准号：
3129093
负责人：
EDWARD L. MORGAN
金额：
$ 9.93万
依托单位：
SCRIPPS CLINIC AND RESEARCH FOUNDATION
依托单位国家：
美国
项目类别：
财政年份：
1983
资助国家：
美国
起止时间：
1983-01-01 至 1986-12-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3129093
关键词：
B lymphocyte T lymphocyte anaphylatoxins cell cell interaction cellular immunity humoral immunity immunoregulation immunosuppression interleukin 2 leukocyte activation /transformation macrophage monocyte tissue /cell culture

项目摘要

The long term goal of this proposal is to investigate the role of complement-derived anaphylatoxins, C3a and C5a, in regulation of human cell-mediated and humoral immunity. Preliminary studies indicate that C3a can suppress and C5a can enhance specific and nonspecific humoral immune responses. The proposed studies have been designed to ascertain the anaphylatoxin-cell and cell-cell interactions involved in anaphylatoxin-mediated regulation of the immune response. A comprehensive study will be conducted to define the cellular levels of C3a and C5a action. The requirement for accessory cells and the nature of signals provided by these cells will be extensively investigated. The fact that active synthetic peptides based on the C3a structure are known, will permit us to examine the active site of C3a as possible mediators of suppression. The possibility that anaphylatoxin-mediated immune regulation occurs through cytokine production will be examined. Studies on the regulation of the immune response by C3a and C5a will not only lead to a better understanding of lymphocyte activation, but also how complement components are involved in the cellular and subcellular events leading to immune regulation. These studies could lead to clinically valuable insight(s) such as how to use synthetic analogs or soluble factors derived from anaphylatoxin activated cells to modulate autoimmune diseases and as potential immunotherpeutic agents in cancer management.

该提议的长期目标是调查补体过敏性过敏毒素，C3A和C5A，调节人细胞介导的和体液免疫。初步研究表明C3A 可以抑制，C5A可以增强特定和非特异性的体液免疫回答。拟议的研究旨在确定过敏毒素细胞和细胞 - 细胞相互作用过敏毒素介导的免疫反应调节。全面将进行研究以定义C3A和C5A的细胞水平行动。辅助单元的要求和信号的性质这些细胞提供的将进行广泛研究。事实基于C3A结构的主动合成肽是已知的，将允许我们要检查C3A的主动部位，作为可能的抑制介质。过敏毒素介导的免疫调节的可能性发生在通过细胞因子的产生将检查。关于调节的研究 C3A和C5A的免疫反应不仅会导致更好了解淋巴细胞激活，也了解如何补充成分参与细胞和亚细胞事件，导致免疫规定。这些研究可能导致临床上有价值的见解例如如何使用合成类似物或从过敏毒素活化细胞调节自身免疫性疾病，AS 癌症管理中的潜在免疫疗法。