Interleukin 4 (IL-4), Interleukin 5 (IL-5), Interleukin 9 (IL-9), Interleukin 13 (IL-13), Tumor necrosis factor alpha (TNF-alpha), and Interleukin 17A (IL-17A) (IL-4, IL-5, IL-9, IL-13, TNF-alpha, IL-17A)

This target entry represents a collection of six distinct cytokines—Interleukin 4 (IL-4), IL-5, IL-9, IL-13, Tumor Necrosis Factor alpha (TNF-alpha), and Interleukin 17A (IL-17A)—that function as pivotal mediators in inflammatory and autoimmune signaling. IL-4 and IL-13 are central to Type 2 (Th2) immune responses, driving IgE production and airway hyperresponsiveness, while IL-5 is the primary regulator of eosinophil recruitment and activation (Gandhi et al., 2016, Expert Rev Clin Immunol; Varricchi et al., 2017, Front Med). IL-9 is involved in mast cell growth and mucus production, and IL-17A is a hallmark of Th17-mediated inflammation, crucial for host defense and the pathogenesis of psoriasis (Goswami & Kaplan, 2011, J Interferon Cytokine Res; McInnes et al., 2014, Nat Rev Rheumatol). TNF-alpha is a master pro-inflammatory cytokine that triggers systemic inflammatory cascades and is a major driver of joint and gut inflammation (Kalliolias & Ivashkiv, 2016, Nat Rev Rheumatol). These cytokines are targeted by a wide range of approved biologics, such as dupilumab (IL-4/13), mepolizumab (IL-5), adalimumab (TNF-alpha), and secukinumab (IL-17A), to treat chronic conditions including asthma, atopic dermatitis, rheumatoid arthritis, and psoriasis.

Other names

Type 2 CytokinesPro-inflammatory CytokinesTh2/Th17 Cytokine PanelB-cell stimulatory factor 1 (IL-4)Eosinophil differentiation factor (IL-5)P600 (IL-13)Cachectin (TNF-alpha)CTLA-8 (IL-17A)

Monoclonal antibodies or fusion proteins that bind to and neutralize the soluble cytokine ligands or their specific cell-surface receptors, thereby inhibiting downstream signaling pathways such as JAK-STAT, NF-kappaB, and MAPK (Gandhi et al., 2016; Kalliolias & Ivashkiv, 2016).