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[Comment] Interleukin 23 inhibitors for psoriasis: not just another number

Major advances have been made in the past 30 years in elucidating the pathogenesis of psoriasis, including the identification of T-helper 17 (Th17) lymphocytes as key players in psoriatic inflammation. Th17 lymphocytes are pathogenetic mainly through the release of their effector cytokine, interleukin 17.1 Although Th17 cells infiltrating psoriatic plaques release other pathogenetic cytokines, such as interleukin 22, the clinical development of several effective interleukin 17 inhibitors—including secukinumab and ixekizumab, which have been licensed for use in moderate-to-severe psoriasis—provided an enlightening demonstration of this model of pathogenesis.

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