On the production of TNF-related apoptosis-inducing ligand (TRAIL/Apo-2L) by human neutrophils

促炎细胞因子 生物 肿瘤坏死因子α 趋化因子 细胞生物学 炎症 免疫学 效应器 细胞因子 自身免疫 Fas配体 细胞凋亡 免疫系统 程序性细胞死亡 遗传学
作者
Marco A. Cassatella
出处
期刊:Journal of Leukocyte Biology [Oxford University Press]
卷期号:79 (6): 1140-1149 被引量:51
标识
DOI:10.1189/jlb.1005558
摘要

Abstract Contrary to their traditional characterization as terminally differentiated effectors of inflammation, neutrophils are remarkably versatile cells. Indeed, their capacity to change phenotype under specific circumstances, their active involvement in the regulation and resolution of inflammation, their response to a wide variety of cytokines and chemotactic molecules, and their regulatory role in angiogenesis and tumor fate have made it clear that they represent far more than “short-lived cells devoid of transcriptional activities, that only release preformed mediators and kill pathogens”. The multiple and amazing functional capacities of this cell type are also illustrated by the fact that the neutrophil may function as an important source of cytokines, at levels comparable with and in some cases, higher than those made by other leukocytes. To date, the families of cytokines, which in vitro or in vivo have been convincingly reported as being produced by neutrophils, include proinflammatory/anti-inflammatory cytokines, immunoregulatory cytokines, chemokines, angiogenic/fibrogenic factors, and tumor necrosis factor (TNF) superfamily members. The latter molecules are multifaceted cytokines whose integrated actions not only influence the development, homeostasis, and adaptive responses of many cells and tissue types but are also implicated in the antitumoral response. The recent findings that neutrophils produce in a finely regulated manner a TNF superfamily member involved in tumor cell killing and autoimmunity, namely TNF-related apoptosis-inducing ligand, open an additional perspective to exploit neutrophils for novel roles in anticancer responses and modulation of autoimmune diseases.
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