Complement peptides and mast cell triggering

Complement peptides and mast cell triggering
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DOI:
10.1016/s0165-2478(96)02658-2
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发表时间:
1996-12-01
期刊:
影响因子:
4.4
通讯作者:
Pecht, I
Pecht, I
中科院分区:
医学3区
文献类型:
--
作者:
Erdei, A;Pecht, I

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早期已证明粘膜型肥大细胞对阳离子剂(例如过敏毒素、神经肽或多胺)提供的所谓“肽能”刺激没有反应。我们研究了肥大细胞的分泌反应之间的关系,刺激通过其1型Fc ε受体(Fc ε RI)和补体系统的C5 a和C3 a片段,在大鼠粘膜型肥大细胞系RBL-2 H3。我们的研究结果揭示了C3 a的一种新功能,即其对IgE介导的粘膜肥大细胞触发的抑制能力。C3 a的这种活性最可能是通过其与Fc β RI的β链的相互作用介导的。虽然已知结缔组织型肥大细胞被微摩尔浓度的补体肽C3 a和C5 a激活,但在我们的测定中抑制抗原诱导的粘膜细胞脱粒所需的C3 a的量在纳摩尔范围内。有趣的是,已知在几种生物测定中更有效的另一种过敏毒性肽C5 a在相同的测试系统中没有显示出任何活性。(C)1996年Elsevier Science B.V.
Mucosal type mast cells have been earlier shown to be unresponsive to the so called 'peptidergic' stimulus provided by cationic agents, such as anaphylatoxins, neuropeptides or polyamines. We studied the relationship between mast cells' secretory response to stimulation via their type 1 Fc epsilon receptors (Fc epsilon RI) and that provided by C5a and C3a fragments of the complement system, in the rat mucosal-type mast cell line RBL-2H3. Our results shown here reveal a novel function of C3a, its inhibitory capacity on IgE-mediated triggering of mucosal mast cells. This activity of C3a is most probably mediated by its interaction with the beta-chain of Fc epsilon RI. While connective tissue type mast cells are known to be activated by micromolar concentrations of the complement peptides C3a and C5a, the amount of C3a necessary for the inhibition of antigen-induced degranulation of mucosal cells in our assays is in the nanomolar range. Interestingly, the other anaphylatoxic peptide C5a, which is known to be much more effective in several biological assays, did not show any activity in the same test-system. (C) 1996 Elsevier Science B.V.