TNFalfa

TNFalfa is a reference to tumor necrosis factor alpha, a cytokine central to the regulation of immune and inflammatory responses. While the standard term in scientific literature is TNF-α (or TNF alpha), the form TNFalfa is encountered in some discussions and nonstandard spellings. TNF-α belongs to the tumor necrosis factor (TNF) superfamily and acts as a key mediator of inflammation.

TNF-α is produced primarily by activated macrophages, but also by T cells, natural killer cells, and adipocytes, in response to infection or immune stimuli. It promotes inflammation, stimulates the production of other cytokines, and supports fever and the acute phase response. Depending on context, it can also induce cell death or contribute to tissue damage in chronic inflammatory states.

Mechanistically, TNF-α signals through two receptors, TNFR1 (CD120a) and TNFR2 (CD120b). TNFR1 is widely expressed, while TNFR2 is more restricted to immune and some endothelial cells. Signaling can activate NF-κB and MAPK pathways, driving inflammation and cell survival, or trigger caspase cascades leading to apoptosis, with outcomes shaped by cellular context and co-stimulatory signals.

Clinical relevance includes associations between TNF-α dysregulation and autoimmune and inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis, and ankylosing spondylitis, as well as septic shock in severe infections. Therapeutically, anti-TNF agents—including monoclonal antibodies infliximab, adalimumab, and golimumab; the soluble receptor etanercept; and certolizumab pegol—are used to treat these conditions. Side effects can include infection risk and reactivation of latent tuberculosis, necessitating appropriate patient monitoring.