Inhibition of IgE-mediated triggering of mast cells by complement-derived peptides interacting with the FcεRI

被引：15

作者：

Erdei, A

Tóth, GK

Andrásfalvy, M

Matkó, J

Bene, L

Bajtay, Z

Ischenko, A

Rong, X

Pecht, I

机构：

[1] Eotvos Lorand Univ, Dept Immunol, Res Grp, Hungarian Acad Sci, H-2131 God, Hungary

[2] Albert Szent Gyorgyi Med Sch, Dept Med Chem, Szeged, Hungary

[3] Sch Med, Dept Biophys & Cell Biol, Debrecen, Hungary

[4] Res Inst Highly Pure Biochem, St Petersburg, Russia

[5] Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel

来源：

IMMUNOLOGY LETTERS | 1999年 / 68卷 / 01期

关键词：

bone marrow derived mast cells; C3a; beta-chain of Fc epsilon RI; inhibition of IgE-mediated triggering; RBL-2H3; cells;

D O I：

10.1016/S0165-2478(99)00033-4

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Mucosal type mast cells, in contrast to the serosal type ones, do not respond to cationic agents, or to the complement-derived peptides C3a and C5a [1]. Earlier we have found that while C3a does not activate the rat mucosal type mast cells (line RBL-2H3), it strongly inhibits the IgE-mediated triggering of these cells, by interfering with the Fc epsilon RI-initiated signaling pathway [2]. In the present study we further investigated the mechanism of this process. It is shown, that C3a interacts with the beta-chain of the Fc epsilon RI complex. Binding of the complement peptide to the cells apparently causes a decrease in the proximity of the IgE-binding Fc epsilon RI. Investigating certain sequences of C3a we found that the inhibition is caused by the C-terminal sequences of the complement-peptide, ranging from positions 56 to 77 and also by a shorter sequence, ranging from positions 56 to 64. The inhibitory effect of these peptides was observed both in the case of RBL-2H3 cells and mouse bone marrow derived mast cells. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：79 / 82

页数：4