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October 13, 2021

Targeting Immune Checkpoints and Cytokines to Protect From Psoriasis Relapse

Author Affiliations
  • 1Department of Dermatology, Venereology and Allergology, Charité–Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany
JAMA Dermatol. Published online October 13, 2021. doi:10.1001/jamadermatol.2021.3491

In contrast to the state of the field 10 years ago, the understanding of disease pathogenesis and the treatment goals for patients with psoriasis have changed enormously. A 75% improvement in the Psoriasis Area and Severity Index (PASI 75) is no longer the desirable treatment goal for dermatologists or for disease-experienced patients with plaque-type psoriasis. Physicians and patients now demand a PASI 90 or even a PASI 100. Identification of interleukin (IL)–17 and IL-23 as key mediators in the pathogenesis of psoriasis and the development of new biologics that target these pathways are major steps toward disease control.1 By targeting cytokines, a clear or almost clear disease status became an achievable goal in a substantial number of patients. The molecular and cellular mechanisms that underlie disease milestones in psoriasis treatment have not yet been fully elucidated, and we remain far from a permanent cure. In particular, we are missing the biomarkers and molecular indicators of forthcoming psoriasis flares in patients who show no or minimal disease activity. This is critical information for identifying the appropriate point in time to discontinue a systemic medication in an individual who has achieved disease control.

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