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When bugs and drugs conspire: driving acneiform skin toxicity
Allison C. Billi, … , Mrinal K. Sarkar, Johann E. Gudjonsson
Allison C. Billi, … , Mrinal K. Sarkar, Johann E. Gudjonsson
Published February 4, 2020
Citation Information: J Clin Invest. 2020;130(3):1090-1092. https://doi.org/10.1172/JCI133787.
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Commentary

When bugs and drugs conspire: driving acneiform skin toxicity

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Abstract

Therapy with antineoplastic agents that inhibit EGFR and MEK is frequently limited by cutaneous adverse reactions, most commonly acne-like eruptions. In this issue of the JCI, Satoh et al. define a mechanism for acneiform skin toxicity wherein EGFR/MEK inhibitors cooperate with the skin commensal Cutibacterium acnes to induce IL-36γ in keratinocytes via the combined actions of Krüppel-like factor 4 and NF-κB transcription factors at the IL-36γ promoter, resulting in neutrophil recruitment. In addition to elucidating why EGFR/MEK inhibitor–induced rashes are often pustular and folliculocentric, this mechanism provides justification for the long-standing practice of management with antibiotic therapy.

Authors

Allison C. Billi, Mrinal K. Sarkar, Johann E. Gudjonsson

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