Our increasing understanding of cellular "corpse" generation and elimination  has contributed immensely to our appreciation of the scope of innate immune function. The concept of physiological cell death emerged from studies of animal development during the latter half of the 19lh century . However, the idea that a cell can activate a suicidal program of self-destruction (programmed cell death), which can be modified by external signals has only been developed during the last half of the 20lh century, and this was considered essential for the development, homeostasis and integrity of multicellular organisms , The description of cell death by apoptosis in the early 1970's provided a phenotype which became a focus for the investigation of homeostatic, 'physiological' cell death (cellular homeostasis) in normal and pathological tissues (e.g. cancer regression) , Apoptosis was viewed as a prelude to the orderly removal of the non-viable cells by phagocytosis in the absence of inflammation. The molecular processes of apoptosis was investigated as an active mechanism of cell death induced by steroids, antibody-dependent cytolysis by lymphocyte killer (K) cells, NK cells and cytotoxic CD8+ T cells consistent with its generalized utility in biology [67, 68].
The science of phagocytosis has undergone a revolution in the last few years from a descriptive to an analytical approach , and combined with advances in cytokine and chemokine research so has our appreciation of innate imunity. The demonstration that while phagocytosis of necrotic cells, clearly a danger signal, produces an inflammatory response, phagocytosis of apoptotic cells does not, provided further support for Matzinger's "danger"' hypothesis. Phagocytosis of apoptotic cells which have undergone a process of programmed cell death is at the core of many biological processes, pathological or physiological, which depend on the innate immune system.
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