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These four cytokines—tumor necrosis factor alpha, interleukin 6, interleukin 17A, and interleukin 17F—are central mediators of inflammation and immunity. They can interact synergistically to drive the pathogenesis of autoimmune and chronic inflammatory diseases, and are individual targets for therapeutic biologic agents. Their blockade is effective in reducing symptoms and progression of diseases such as rheumatoid arthritis, psoriasis, and asthma, but may increase risk of infection due to their roles in host defense[1][3][5][4][6][2].
Therapeutic mechanisms involve neutralization of cytokine activity or antagonism of their respective receptors, leading to suppression of downstream inflammatory signaling pathways. This can include inhibition of binding, receptor antagonism, or dual inhibition for related family members.
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