Tumour Necrosis Factor alpha (TNF-a), also known as cachectin was initially named for its remarkable ability to cause hemorrhagic necrosis of tumours in mice.1 The TNF-a gene located on chromosome 6 encodes a 233 amino acid (a.a.) prohormone bound to the plasma membrane, with the mature form (157a.a., 17kDa) exposed on the extracellular surface. Soluble, mature TNF-a is released upon cleavage of the C-terminal.2,3 The primary source in vivo of TNF-a is thought to be the monocyte/macrophage but various cell types are known to express this cytokine such as lymphocytes, basophils, eosinophils, mast cells, NK cells, T cells, B cells, kerantinocytes, Kupffer cells, astrocytes, and some types of tumours. TNF-a is produced upon stimulation with cytokines such as IL-1, 1L-2, GM-CSF, TNF-a itself and with bacterial lipopolysaccharide (LPS) which is a potent inducer.4 TNF-a once produced and secreted will bind to TNF-a receptors (TNF-a R1, 55 kDa and TNF-a R2, 75 kDa), located on the plasma membrane of most cells throughout the body except the red blood cell.5 The two TNF-a receptors deliberate the biological effects of TNF-a. It has been reported that TNF-a R1 is responsible for mediating LPS toxicity6 and cell cytotoxicity7 and TNF-a R2 is involved in cellular proliferation.8 Various pathological conditions are associated with the production of high levels of TNF-a. These include septic shock syndrome, cachexia (e.g. HIV, tuberculosis, cancer), autoimmune diseases, hepatitis, leukemia, myocardial ischaemia, organ transplantation rejection, multiple sclerosis, rheumatoid arthritis, and meningococcal septicemia.4,9,10,11 Many people die annually from a complication of infectious disease called septic shock syndrome which is triggered by TNF-a. In many cases elevated TNF-a serum levels predict a higher mortality.12 TNF-a is a pleiotropic cytokine that can induce disease through TNF-a toxicity (tissue injury, catabolic illness, and mediating shock) and improve host defense mechanisms (stimulating inflammation and increasing immune cell function).4 In the future, therapies may be developed by blocking TNF-a harmful effects and enhancing TNF-a beneficial effects. This TNF-a ELISA is a 2.5-3 hour solid phase immunoassay readily applicable to measure TNF-a levels in serum, plasma, cell culture supernatant, and other biological fluids in the range of 0 to 1000 pg/mL. It showed no cross reactivity with other cytokines tested.