Interleukin 3-dependent mediator release in basophils triggered by C5a.

摘要: The anaphylatoxin C5a is a potent trigger for basophil degranulations, but in contrast to IgE-dependent activation, it does not result the synthesis of sulfidoleukotrienes (leukotriene C4/D4/E4). Thus, degranulation and generation lipid mediators are separately regulated cellular responses. Exposure human blood basophils cytokine IL-3 alone induce release histamine cells from most donors never leads LTC4, indicating that direct agonist mediator release. However, preincubation with enhances response C5a. Most importantly, "primes" large amounts leukotriene C4 after challenge (mean 50 gp LTC4 per nanograms histamine), while neither peptide capable inducing formation bioactive lipids. This effect dose dependent, occurring at concentrations considerably lower than required stimulate growth bone marrow progenitor cells. affects extent time course degranulation, sequentially exposed occurs very rapidly concomitant degranulation. A strictly C5a-induced synthesis, an enhancement Priming exposure IL-3, starting 1 min reaching maximal effects 5 min, this altered state responsiveness relatively long lasting. Cell fractionation studies indicate source directly. study demonstrates modifier effector functions mature basophils; possibly greater vivo significance its factor properties. formed triggering IL-3-primed may only enhance also qualitatively change pathophysiological consequences complement might be important pathogenesis immediate type hypersensitivity reactions, shock syndromes, inflammation.