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表面结合IgG介导的中性粒细胞激活:百日咳毒素不敏感的激活作用

Neutrophil activation by surface bound IgG: pertussis toxin insensitive activation.

作者信息

Blackburn W D, Heck L W

机构信息

Department of Medicine, University of Alabama, Birmingham 35294.

出版信息

Biochem Biophys Res Commun. 1988 Apr 15;152(1):136-42. doi: 10.1016/s0006-291x(88)80690-9.

Abstract

Surface bound IgG induces neutrophil degranulation and production of superoxide radicals by a mechanism that is not inhibited by either pertussis toxin or cholera toxin, whereas these functions induced by soluble mediators such as FMLP and soluble aggregates of IgG are profoundly inhibited by pertussis toxin. Interaction of neutrophils with surface bound IgG triggers the loss of 32P labeled PIP2 and PIP and the influx of extracellular calcium. Neither of these cellular events when induced by surface bound IgG is inhibited by pertussis toxin. These observations suggest that neutrophil activation induced by surface bound IgG proceeds along a pathway which is not regulated by proteins which are inhibited by either pertussis or cholera toxins.

摘要

表面结合的IgG通过一种既不受百日咳毒素也不受霍乱毒素抑制的机制诱导中性粒细胞脱颗粒和超氧自由基的产生,而由可溶性介质如FMLP和IgG可溶性聚集体诱导的这些功能则受到百日咳毒素的强烈抑制。中性粒细胞与表面结合的IgG相互作用会触发32P标记的PIP2和PIP的丢失以及细胞外钙的内流。由表面结合的IgG诱导的这些细胞事件均不受百日咳毒素的抑制。这些观察结果表明,表面结合的IgG诱导的中性粒细胞活化是沿着一条不受百日咳或霍乱毒素抑制的蛋白质调节的途径进行的。

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