Loading…

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

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 trigge...

Full description

Saved in:
Bibliographic Details
Published in:Immunology letters 1999-05, Vol.68 (1), p.79-82
Main Authors: Erdei, Anna, K. Tóth, Gábor, Andrásfalvy, Márton, Matkó, János, Bene, László, Bajtay, Zsuzsa, Ischenko, Alexander, Rong, Xu, Pecht, Israel
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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 FcεRI-initiated signaling pathway [2]. In the present study we further investigated the mechanism of this process. It is shown, that C3a interacts with the β-chain of the FcεRI complex. Binding of the complement peptide to the cells apparently causes a decrease in the proximity of the IgE-binding FcεRI. 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.
ISSN:0165-2478
1879-0542
DOI:10.1016/S0165-2478(99)00033-4