Simon Hans-Uwe
Department of Pharmacology, University of Bern, Switzerland.
Chem Immunol Allergy. 2006;91:49-58. doi: 10.1159/000090229.
Apoptosis is the most common form of physiological cell death and a necessary process to maintain cell numbers in multicellular organisms. Eosinophils are constantly produced in the bone marrow and the same numbers die, under normal circumstances, within a relatively short time period. In many eosinophilic inflammatory diseases, reduced eosinophil apoptosis has been described. This mechanism may contribute to increased eosinophil numbers, a phenomenon called eosinophilia. Overexpression of interleukin-5 appears to be crucial for delaying eosinophil apoptosis in many allergic disorders. Survival factor withdrawal leads to the induction of apoptosis. Besides survival cytokines, eosinophil apoptosis is also regulated by death factors. Recent observations suggest a role for mitochondria in conducting eosinophil apoptosis, although the mechanisms that trigger mitochondria to release proapoptotic factors remain less clear. Drugs that specifically induce eosinophil apoptosis might be useful for triggering the resolution of unwanted eosinophilic inflammatory responses.
细胞凋亡是生理性细胞死亡的最常见形式，也是多细胞生物体维持细胞数量的必要过程。嗜酸性粒细胞在骨髓中持续产生，在正常情况下，相同数量的嗜酸性粒细胞会在相对较短的时间内死亡。在许多嗜酸性粒细胞炎症性疾病中，已发现嗜酸性粒细胞凋亡减少。这种机制可能导致嗜酸性粒细胞数量增加，即嗜酸性粒细胞增多现象。在许多过敏性疾病中，白细胞介素-5的过度表达似乎对延迟嗜酸性粒细胞凋亡至关重要。生存因子的撤除会导致细胞凋亡的诱导。除了生存细胞因子外，嗜酸性粒细胞凋亡还受死亡因子的调节。最近的观察结果表明线粒体在嗜酸性粒细胞凋亡过程中发挥作用，尽管触发线粒体释放促凋亡因子的机制仍不太清楚。特异性诱导嗜酸性粒细胞凋亡的药物可能有助于引发不必要的嗜酸性粒细胞炎症反应的消退。
