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001-es BibID:	BIBFORM004646
Első szerző:	Erdei Anna
Cím:	Inhibition of IgE-mediated triggering of mast cells by complement-derived peptides interacting with the Fc epsilon RI / Erdei, A., Toth, G. K., Andrasfalvy, M., Matko, J., Bene, L., Bajtay, Z., Ischenko, A., Rong, X., Pecht, I.
Dátum:	1999
Megjegyzések:	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. 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. 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
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Amino Acid Sequence Animal Bone Marrow Cells Cells Cells,Cultured chemistry Complement Complement 3a Hungary Immunoglobulin E immunology Immunosuppressive Agents Mast Cells metabolism Mice Molecular Sequence Data Peptides pharmacology physiology Protein Conformation Rats Receptors, IgE Support, Non-U.S.Gov't
Megjelenés:	Immunology Letters. - 68 : 1 (1999), p. 79-82. -
További szerzők:	Tóth Gábor K. Andrásfalvy Márton Matkó János (1952-) (biológus) Bene László (1963-) (biofizikus) Bajtay Zsuzsa Ischenko, Alexander Rong, Xu Pecht, Israel
Internet cím:	DOI elektronikus változat elektronikus változat
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