Macrophage cytotoxin

TNF-a is also known as cachectin, macrophage cytotoxic factor, macrophage cytotoxin and necrosin. As some of these names suggest, activated macrophages appear to represent the most significant cellular source of TNF-a, but it is also synthesized by many other cell types (Table 9.5). Producer cells do not store TNF-a, but synthesize it de novo following activation. 

Activated T cells produce cytotoxins, which are directly toxic to tissues, and cytokines, which stimulate further activation of inflammatory processes and attract cells to areas of inflammation. Macrophages are stimulated to release prostaglandins and cytotoxins. 

Tumour necrosis factor (TNF) was originally described as a factor produced following exposure of Bacille-Calmette-Guerin-treated animals to bacterial endotoxin. It was so named because it possessed the ability to necrotise tumours. This factor is now named TNF-a to distinguish it from another, related cytokine lymphotoxin, which is sometimes referred to as TNF-/J Alternative names for TNF-a include cachectin and cytotoxin. Its primary cellular source in the body is the activated macrophage, but some other cell types (e.g. NK cells, astrocytes, some lymphocytes, fibroblasts, many tumour cells, endothelial cells and neutrophils) have also been shown to synthesise this cytokine. 

The pathogenesis of RA is a combination of cellular (e.g., macrophages, lymphocytes), biochemical (e.g., prostaglandins, cytotoxins) and mechanical factors that promote the inflammatory condition of the synovial lining. The normal anatomy... 

Alvarez, M. N., G. Peluffo, L. Piacenza, and R. Radi. 2011. Intraphagosomal peroxynitrite as a macrophage-derived cytotoxin against internalized Trypanosoma cruzi Consequences for oxidative killing and role of microbial peroxiredoxins in infectivity. 

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