Abstract
The role of the interleukin (IL)23/IL17 axis in psoriasis is well-established and has led to the development of biologics targeting IL23 and IL17A. Ustekinumab, targets the IL12/23p40 shared subunit and blocks IL23-receptor interactions, restricting the activation of Signal Transducer and Activator of Transcription 3 (STAT3) in T cells, and IL17A production. Secukinumab blocks IL17A binding to its receptor, preventing keratinocyte activation. Although both biologics are effective, clinical response varies, highlighting the need to identify biomarkers predictive of response.
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