Zhang Y, Ramos B F, Jakschik B A
Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110.
Science. 1992 Dec 18;258(5090):1957-9. doi: 10.1126/science.1470922.
During generalized immune complex-induced inflammation of the peritoneal cavity, two peaks of tumor necrosis factor (TNF) were observed in the peritoneal exudate of normal mice. In mast cell-deficient mice, the first peak was undetected, and the second peak of TNF and neutrophil influx were significantly reduced. Antibody to TNF significantly inhibited neutrophil infiltration in normal but not in mast cell-deficient mice. Mast cell repletion of the latter normalized TNF, neutrophil mobilization, and the effect of the antibody to TNF. Thus, in vivo, mast cells produce the TNF that augments neutrophil emigration.
在全身性免疫复合物诱导的腹腔炎症过程中，在正常小鼠的腹腔渗出液中观察到肿瘤坏死因子（TNF）出现两个峰值。在肥大细胞缺陷小鼠中，第一个峰值未被检测到，并且TNF的第二个峰值和中性粒细胞流入显著减少。抗TNF抗体显著抑制正常小鼠而非肥大细胞缺陷小鼠中的中性粒细胞浸润。对后者进行肥大细胞补充可使TNF、中性粒细胞动员以及抗TNF抗体的作用恢复正常。因此，在体内，肥大细胞产生增强中性粒细胞迁移的TNF。
