IL-17 inhibitors effectively alleviate joint inflammation and bone destruction by specifically neutralizing the pro-inflammatory factor IL-17, but their single-target mechanism limits their ability to regulate the immune microenvironment as a whole; TNF-α inhibitors can rapidly inhibit the key inflammatory mediator TNF-α to improve symptoms, but long-term use may increase the risk of opportunistic infections and malignant tumors due to systemic immune suppression. The gene discussed is IL17A; the disease is Opportunistic infection.