Tumor necrosis factor and interleukin-17A (TNF and IL-17A) (TNF/IL-17A)

Tumor necrosis factor (TNF) and interleukin-17A (IL-17A) are potent pro-inflammatory cytokines that play central roles in the pathogenesis of various autoimmune and inflammatory diseases (NIH, 2015). While TNF is a primary mediator of systemic inflammation and synovial tissue damage, IL-17A is crucial for neutrophil recruitment and the maintenance of chronic inflammation, particularly at entheseal sites (Frontiers in Immunology, 2019). These two cytokines exhibit a powerful biological synergy, where their combined presence leads to a significantly greater induction of inflammatory mediators like IL-6 and IL-8 than either cytokine alone (NIH, 2015). Dual targeting of TNF and IL-17A is a therapeutic strategy designed to provide more comprehensive disease control, especially for patients who do not achieve adequate responses with single-cytokine inhibitors (mAbs, 2016). Bispecific molecules such as ABT-122 and COVA322 have been developed to neutralize both targets simultaneously, aiming to improve clinical outcomes in conditions such as rheumatoid arthritis and psoriatic arthritis (Arthritis & Rheumatology, 2018). However, the strategy must balance increased efficacy with the potential for heightened risks of infection, such as candidiasis and tuberculosis (NIH, 2017).

Other names

TNF-alpha and IL-17ATumor necrosis factor alpha and interleukin 17ATNF and IL-17A dual targetTNF/IL-17A combination

Simultaneous neutralization of the pro-inflammatory cytokines TNF and IL-17A to inhibit synergistic signaling pathways and reduce tissue destruction.