Erdei A, Kerekes K, Pecht I
Department of Immunology, University L. Eötvös, Göd, Hungary.
Exp Clin Immunogenet. 1997;14(1):16-8.
Mast cells and basophils are known to be triggered by allergens via cross-linking with their high-affinity IgE-binding receptors, Fc epsilon RI. The anaphylatoxic activity of the complement-derived peptides C3a and C5a has been known for a long time; however, it has also been reported that serosal- and mucosal-type mast cells respond differently to peptidergic stimuli. The mechanism of mast cell activation by cross-linking of Fc epsilon RI has been the subject of intensive studies in the past few years, while the action mode of the anaphylatoxic complement peptides has been revealed only recently. We report about a novel function of C3a: its inhibitory activity on IgE-mediated triggering of the mucosal RBL-2H3 cells. Surprisingly, the other anaphylatoxic peptide C5a, which has been shown to be significantly more effective in several biological assays, did not influence antigen-induced triggering of the RBL-2H3 cell line at all.
众所周知,肥大细胞和嗜碱性粒细胞可通过与它们的高亲和力IgE结合受体FcεRI交联而被过敏原触发。补体衍生肽C3a和C5a的过敏毒素活性早已为人所知;然而,也有报道称,浆膜型和粘膜型肥大细胞对肽能刺激的反应不同。在过去几年中,FcεRI交联激活肥大细胞的机制一直是深入研究的主题,而过敏毒素补体肽的作用模式直到最近才被揭示。我们报道了C3a的一种新功能:它对IgE介导的粘膜RBL-2H3细胞触发具有抑制活性。令人惊讶的是,另一种过敏毒素肽C5a在几种生物学检测中已被证明效力显著更强,但它对RBL-2H3细胞系的抗原诱导触发根本没有影响。