Endotoxin priming of monocytes augments Fc gamma receptor cross-linking-induced TNF-alpha and IL-1 beta release.
Endotoxin priming of monocytes augments Fc gamma receptor cross-linking-induced TNF-alpha and IL-1 beta release.
复制标题
单核细胞的内毒素引发增强 Fc γ 受体交联诱导的 TNF-α 和 IL-1 β 释放。
DOI：
10.1152/ajplung.1993.265.2.l178
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Wewers,MD
中科院分区：
文献类型：
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作者：
Kindt,GC;Moore,SA;She,ZW;Wewers,MD
免疫球蛋白G(Ig G)Fc区的交联型受体(Fc-Gamma R)可诱导肿瘤坏死因子-α(TNF-α)的释放，但对IL-1β的释放存在争议。本研究的目的是探讨内毒素对Fc-Gamma-R交联后单核细胞释放这些细胞因子能力的影响。单核细胞与平板或可溶性人免疫球蛋白或白蛋白共同孵育，并加或不加内毒素。Percoll分离的含有低浓度内毒素的单核细胞，在平板抗体上孵育后，释放4.5+/-1.6 ng/mlTNF-α和1.6+/-0.6 ng/mlIL-1β。通过“聚集”技术分离的单核细胞释放1.0+/-0.4 ng/mlTNF-α，但不释放IL-1β。用不影响Fc-Gamma R表达的内毒素刺激单核细胞，与单纯白蛋白孵育的单核细胞相比，单核细胞分泌的肿瘤坏死因子-α(4.3+/-1.3vs.0.1+/-0.0 ng/ml，P<0.05)和IL-1β(4.0+/-1.0vs.0.6+/-0.3 ng/ml，P<；0.01)增加。
Cross-linking receptors for the Fc region of immunoglobulin G (IgG) (Fc gamma R) induces tumor necrosis factor-alpha (TNF-alpha) release; however, there is controversy about release of interleukin (IL)-1 beta. The purpose of this study was to investigate the role of endotoxin priming on the ability of monocytes to release these cytokines after Fc gamma R cross-linking. Monocytes were incubated with plated or soluble human IgG or albumin with or without endotoxin priming. Monocytes isolated by Percoll, containing low concentrations of endotoxin, and incubated on plated IgG released 4.5 +/- 1.6 ng/ml TNF-alpha and 1.6 +/- 0.6 ng/ml IL-1 beta. Monocytes isolated by a “clumping” technique released 1.0 +/- 0.4 ng/ml TNF-alpha but no IL-1 beta. Priming with endotoxin, which did not affect Fc gamma R expression, resulted in augmented release of TNF-alpha (4.3 +/- 1.3 vs. 0.1 +/- 0.0 ng/ml, P < 0.05) and IL-1 beta (4.0 +/- 1.0 vs. 0.6 +/- 0.3 ng/ml, P < 0.01) when clumped monocytes were incubated on plated IgG vs. plated albumin.