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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?
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...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6023723/ https://www.ncbi.nlm.nih.gov/pubmed/29704872 http://dx.doi.org/10.1111/exd.13676 |
Sumario: | 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. |
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