호산구 세포자멸사
Eosinophil Apoptosis
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초록
Eosinophilia is common feature in many diseases, including allergic diseases. There are many factors involved in the survival and the death of eosinophil. Apoptosis is the most common form of physiological cell death and a necessary process to maintain cell numbers in multicellular organisms. It has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of eosinophils in tissue. Overexpression of interleukin-5 appears to be crucial for delaying eosinophil apoptosis. Besides survival cytokines, eosinophil apoptosis is also regulated by death factor. Recent observations suggest a role for mitochondria in conducting eosinophil apoptosis, although the mechanisms that trigger mitochondria to release proapoptotic factors remain less clear. Acceleration of eosinophil apoptosis can be achieved by decreased expression of eosinophil survival factors, and promotion of death signals. However, many previous studies on the regulation of apoptosis have utilized cell lines which may not directly represent cells within the in vivo environment. Therefore, the control of eosinophil apoptosis can be another therapeutic strategy in allergic diseases.
Abstract
Eosinophilia is common feature in many diseases, including allergic diseases. There are many factors involved in the survival and the death of eosinophil. Apoptosis is the most common form of physiological cell death and a necessary process to maintain cell numbers in multicellular organisms. It has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of eosinophils in tissue. Overexpression of interleukin-5 appears to be crucial for delaying eosinophil apoptosis. Besides survival cytokines, eosinophil apoptosis is also regulated by death factor. Recent observations suggest a role for mitochondria in conducting eosinophil apoptosis, although the mechanisms that trigger mitochondria to release proapoptotic factors remain less clear. Acceleration of eosinophil apoptosis can be achieved by decreased expression of eosinophil survival factors, and promotion of death signals. However, many previous studies on the regulation of apoptosis have utilized cell lines which may not directly represent cells within the in vivo environment. Therefore, the control of eosinophil apoptosis can be another therapeutic strategy in allergic diseases.
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