TNF-alpha

Class

Anti-TNF inhibitor

Pathway

TNF-α signalling

Tumor necrosis factor-alpha (TNF-α) is a signaling protein, or cytokine, produced mainly by immune cells such as macrophages and T cells during inflammation. Under normal conditions it helps coordinate short-term immune defenses, recruiting other immune cells and inducing fever and tissue changes needed to fight infection or injury. In chronic inflammatory diseases, however, TNF-α is produced persistently and in excess, driving ongoing tissue damage. This is well documented in rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, and inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, where TNF-α perpetuates joint erosion, skin plaque formation, or intestinal ulceration. Blocking TNF-α, either by neutralizing the free cytokine or preventing it from engaging its cell-surface receptors, interrupts this self-sustaining inflammatory cycle and can substantially reduce disease activity across these conditions. This rationale has made TNF-α one of the most extensively targeted pathways in immunology, drugged by monoclonal antibodies, antibody fragments, fusion proteins, and increasingly small molecules. Some newer approaches pair TNF-α blockade with inhibition of a second inflammatory mediator, such as interleukin-17 or interleukin-23, reflecting the observation that several cytokine pathways often act together to sustain chronic inflammation, and that addressing more than one simultaneously may produce broader control than blocking TNF-α alone.