补体衍生肽对肥大细胞激活的调节

Regulation of mast cell activation by complement-derived peptides.

作者信息

Erdei Anna, Andrásfalvy Márton, Péterfy Hajna, Tóth Gábor, Pecht Israel

机构信息

Department of Immunology, Research Group of the Hungarian Academy of Sciences, Eötvös Loránd University, Pázmány Péter s. 1/C, H-1117 Budapest, Hungary.

出版信息

Immunol Lett. 2004 Mar 29;92(1-2):39-42. doi: 10.1016/j.imlet.2003.11.019.

DOI:10.1016/j.imlet.2003.11.019

PMID:15081525

Abstract

It is known for more than 25 years that the complement-derived anaphylatoxic peptides, C3a, C4a and C5a are potent activators of basophils and certain types of mast cells. Although tissue distribution of receptors for C3a and C5a well exceeds myeloid cells, apparently they are not expressed on mucosal type mast cells, consequently these cells are not activated by C3a and C5a. Our results do however demonstrate that C3a and peptides related to this complement activation product are able to inhibit FcRI-clustering induced activation of mucosal type mast cells-such as RBL-2H3 cells and bone-marrow derived mast cells. Based on the current results we propose the presence of separate "activator" and "inhibitor" sequence motifs in C3a which are in balance under physiologic conditions.

摘要

25年多来，已知补体衍生的过敏毒素肽C3a、C4a和C5a是嗜碱性粒细胞和某些类型肥大细胞的有效激活剂。尽管C3a和C5a受体的组织分布远远超过髓样细胞，但显然它们在黏膜型肥大细胞上不表达，因此这些细胞不会被C3a和C5a激活。然而，我们的结果确实表明，C3a以及与这种补体激活产物相关的肽能够抑制FcRI聚集诱导的黏膜型肥大细胞（如RBL-2H3细胞和骨髓来源的肥大细胞）的激活。基于目前的结果，我们提出C3a中存在单独的“激活剂”和“抑制剂”序列基序，它们在生理条件下处于平衡状态。