Tumor necrosis factor alpha, Interleukin-6, Interleukin-1 beta (TNF-α, IL-6, IL-1β)

Tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) are key pro-inflammatory cytokines. Produced mainly by activated macrophages, T cells, and other immune and stromal cells, they orchestrate the acute phase response, drive cellular recruitment and activation (particularly neutrophils and lymphocytes), and stimulate secondary cytokine production. These cytokines are critical for host defense but, when overproduced or chronically activated, they mediate the pathogenesis of numerous inflammatory, autoimmune, metabolic, and degenerative diseases. Importantly, they are individually targeted by specific therapeutics to modulate hyperinflammation[7][1][3][5].

Other names

CachectinTumor necrosis factorInterleukin 6IFN-β2B-cell stimulatory factor-2Interleukin 1 betaCatabolin

Monoclonal antibodies or receptor antagonists block ligand–receptor interactions or neutralize cytokine activity to suppress inflammation (e.g., anti-TNF agents inhibit TNF-α signaling by binding TNF-α; IL-6 receptor blockers inhibit IL-6 signaling; IL-1 receptor antagonists block IL-1β binding[7][1][3]).