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Inhibition of interleukin‐12 and/or interleukin‐23 for the treatment of psoriasis: What is the evidence for an effect on malignancy?
Author(s) -
Ergen Elizabeth N.,
Yusuf Nabiha
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13676
Subject(s) - psoriasis , medicine , context (archaeology) , immune system , immunology , malignancy , interleukin , interleukin 23 , immunotherapy , interleukin 17 , cytokine , biology , paleontology
Abstract Immune cells and cytokines play an important role in the pathogenesis of psoriasis. Interleukin‐12 ( IL ‐12) and IL ‐23 promote cellular responses mediated by T cells, which contribute to an inflammatory loop responsible for the induction and maintenance of psoriatic plaques. Antibodies that inhibit IL ‐12/23 or IL ‐23 are key treatment options for patients with psoriasis. IL ‐12 and IL ‐23 also play a key role in immune responses to infections and tumors. A growing body of information from clinical trials, cohort studies, postmarketing reports, genetic studies and animal models provides insights into the potential biological relationships between IL ‐12/23 inhibition and malignancies. We summarize this information in tables and provide some context for the interpretation of these data with the goal of informing dermatologists who are using IL ‐12/23 or IL ‐23 inhibitors to treat patients with psoriasis.