The Role of Complement Component 3 (C3) in Psoriasis

Psoriasis is a chronic inflammatory disease driven by immune dysfunction, with its pathogenesis still not fully understood. This article explores the crucial roles of complement molecules in psoriasis, emphasizing complement C3's pathogenic mechanisms and its potential as a therapeutic target. The complement system's structure and function highlight its significance in immune response and inflammation regulation. This system is activated through the classical, alternative, and lectin pathways, with complement C3, primarily produced by hepatocytes and macrophages, serving as a core component and the most abundant complement in serum. The article analyzes C3's structure and biological functions to reveal its pathogenic roles in psoriasis, detailing its specific mechanisms in immune abnormalities and skin lesions as supported by recent studies. The activation of the complement system leads to C3 convertase formation, cleaving C3 into C3a and C3b. T cells, though expressing lower C3 levels, produce C3a and C3b, regulating vital T cell functions like CD4+ T cell differentiation and survival. The review also summarizes current therapeutic strategies targeting C3, evaluating their potential effectiveness in alleviating psoriasis symptoms. C3aR inhibitors, such as SB290157, can slow disease progression, proposing a novel therapeutic approach for psoriasis. This comprehensive review offers new insights and theoretical foundations for complement C3 as a target for psoriasis treatment, aiming to advance future research and clinical interventions.