Tumor necrosis factor alpha (TNF-α)

Tumor necrosis factor alpha, or TNF-alpha, is a cytokine released mainly by macrophages that triggers fever, inflammation and the recruitment of immune cells to injured tissue.

It was named for its ability to kill tumor cells in early experiments, but its everyday job is inflammatory signaling. Within minutes of detecting a pathogen, macrophages release TNF-alpha, which acts on blood vessels to make them leaky and sticky, prompts the liver to produce acute-phase proteins, activates NF-kB in surrounding cells and can trigger programmed cell death. Sustained high levels drive rheumatoid arthritis, Crohn's disease, psoriasis and ankylosing spondylitis, and antibody drugs that block TNF-alpha are among the most widely prescribed biologic medicines.

TNF-alpha is measured in blood or in tissue culture as a marker of inflammatory activity. In preclinical CBD studies it is one of the most frequently reported readouts, with reductions described in cells and rodents; such a change is a mechanistic signal rather than evidence of clinical benefit, and human data are limited.