Apoptosis, programmed cell death, of neutrophil and eosinophil granulocytes is a potential control point in the physiological resolution of innate immune responses. There is also increasing evidence that cellular processes of apoptosis can be dysregulated by pathogens as a mechanism of immune evasion and that delayed apoptosis, resulting in prolonged inflammatory cell survival, is important in persistence of tissue inflammation. The identification of cell-type specific pathways to apoptosis may allow the design of novel anti-inflammatory therapies or agents to augment the innate immune responses to infection. This review will explore the physiological roles of granulocyte apoptosis and their importance in infectious and non-infectious lung disease.
Granulocyte apoptosis in the pathogenesis and resolution of lung disease
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Stephen M. Bianchi, David H. Dockrell, Stephen A. Renshaw, Ian Sabroe, Moira K. B. Whyte; Granulocyte apoptosis in the pathogenesis and resolution of lung disease. Clin Sci (Lond) 1 March 2006; 110 (3): 293–304. doi: https://doi.org/10.1042/CS20050178
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