作者: Anna Erdei , Gábor K. Tóth , Márton Andrásfalvy , János Matkó , László Bene
DOI: 10.1016/S0165-2478(99)00033-4
关键词: Cell biology 、 Peptide 、 Signal transduction 、 Ige mediated 、 Biology 、 Interleukin 33 、 Bone marrow 、 Immunology 、 Inhibitory effect 、 Immunology and Allergy
摘要: Abstract Mucosal type mast cells, in contrast to the serosal ones, do not respond cationic agents, or complement-derived peptides C3a and C5a [1]. Earlier we have found that while does activate rat mucosal cells (line RBL-2H3), it strongly inhibits IgE-mediated triggering of these by interfering with FceRI-initiated signaling pathway [2]. In present study further investigated mechanism this process. It is shown, interacts β-chain FceRI complex. Binding complement peptide apparently causes a decrease proximity IgE-binding FceRI. Investigating certain sequences inhibition caused C-terminal complement-peptide, ranging from positions 56 77 also shorter sequence, 64. The inhibitory effect was observed both case RBL-2H3 mouse bone marrow derived cells.