Haslett C
Respiratory Medicine Unit, University Department of Medicine, Royal Infirmary, Edinburgh, UK.
Br Med Bull. 1997;53(3):669-83. doi: 10.1093/oxfordjournals.bmb.a011638.
We have described a novel pathway available for the clearance of extravasated granulocytes whereby the cells undergo apoptosis, a process which controls the functional longevity of granulocytes in situ and the rate of which is modulated by external and internal control mechanisms. It leads to shut-down of the secretory processes and recognition of the intact senescent cell by a novel macrophage recognition mechanism which fails to stimulate the release of pro-inflammatory mediators. Thus, by contrast with a granulocyte fate involving necrosis, apoptosis is likely to represent an injury limiting tissue removal process for granulocytes which would tend to promote resolution processes. It is speculated that dysregulation of this process or an imbalance between it and necrotic pathways may be important in inflammatory disease pathogenesis. Whether or not this is the case, the apoptotic mechanisms available in neutrophil and eosinophil granulocytes provide opportunities for the selective induction of apoptosis in specific inflammatory cells in what may represent novel therapeutic approaches to inflammatory disease.
我们已经描述了一种清除血管外渗粒细胞的新途径,即细胞经历凋亡,这一过程控制着粒细胞在原位的功能寿命,其速率受外部和内部控制机制调节。它导致分泌过程停止,并通过一种新型巨噬细胞识别机制识别完整的衰老细胞,该机制不会刺激促炎介质的释放。因此,与涉及坏死的粒细胞命运相反,凋亡可能代表一种限制粒细胞组织损伤的清除过程,这往往会促进炎症消退。据推测,这一过程的失调或其与坏死途径之间的失衡可能在炎症性疾病发病机制中起重要作用。无论情况是否如此,中性粒细胞和嗜酸性粒细胞中存在的凋亡机制为在特定炎症细胞中选择性诱导凋亡提供了机会,这可能代表了炎症性疾病的新型治疗方法。