Bovine TNF alpha ELISA Kit

Tumor necrosis factor-alpha (TNF-α), also referred to as tumor necrosis factor (TNF), is a cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction. The primary role of TNF is in the regulation of immune cells. TNF is able to induce apoptotic cell death, to induce inflammation, and to inhibit tumorigenesis and viral replication. Dysregulation of TNF production has been implicated in a variety of human diseases, including major depression[1], Alzheimer's disease[2] and cancer.[3]
TNF was originally thought to be produced primarily by macrophages, but it is produced also by a broad variety of cell types including lymphoid cells, mast cells, endothelial cells, cardiac myocytes, adipose tissue, fibroblasts, and neuronal tissue. Large amounts of TNF are released in response to lipopolysaccharide, other bacterial products, and Interleukin-1 (IL-1).

Two receptors, TNF-R1 (TNF receptor type 1; CD120a; p55/60) and TNF-R2 (TNF receptor type 2; CD120b; p75/80), can be bound to by TNF. TNF-R1 is expressed in most tissues, and can be fully activated by both the membrane-bound and soluble trimeric forms of TNF, whereas TNF-R2 is found only in cells of the immune system, and respond to the membrane-bound form of the TNF homotrimer.

Upon contact with their ligand, TNF receptors undergo a conformational change, leading to the dissociation of an inhibitory protein from the intracellular death domain. This dissociation enables the adaptor protein TRADD (tumor necrosis factor receptor type 1-associated death domain) to bind to the death domain, serving as a platform for subsequent protein binding. Following TRADD binding, three pathways can be initiated including activaiton of NF-κB, activation of MAPK pathways, and induction of death signaling.[4][5]

The myriad and often-conflicting effects mediated by these pathways indicate the existence of extensive cross-talk. Other factors, such as cell type, concurrent stimulation with other cytokines, or the amount of reactive oxygen species (ROS) present can shift the balance in favor of one pathway or another. Such complicated signaling ensures that, whenever TNF is released, various cells with vastly diverse functions and conditions can all respond appropriately to inflammation.

Bovine TNF alpha ELISA Catalog No. E11-807
 

 

 
References
1. Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK, Lanctôt KL (2010). "A meta-analysis of cytokines in major depression". Biol Psychiatry 67 (5): 446-457.

2. Swardfager W, Lanctôt K, Rothenburg L, Wong A, Cappell J, Herrmann N (2010). "A meta-analysis of cytokines in Alzheimer's disease". Biol Psychiatry 68 (10): 930-941.

3. Locksley RM, Killeen N, Lenardo MJ (2001). "The TNF and TNF receptor superfamilies: integrating mammalian biology". Cell 104 (4): 487–501.

4. Wajant H, Pfizenmaier K, Scheurich P (2003). "Tumor necrosis factor signaling". Cell Death Differ. 10 (1): 45–65.

5. Chen G, Goeddel DV (2002). "TNF-R1 signaling: a beautiful pathway". Science 296 (5573): 1634–5.

6. Cerami A, Beutler B (1988). "The history, properties, and biological effects of cachectin". Biochemistry 27 (20): 7575–7582.

7. Vilcek J, Lee TH (1991). "Tumor necrosis factor. New insights into the molecular mechanisms of its multiple actions". J. Biol. Chem. 266 (12): 7313–7316.