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.

中文翻译：

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当虫子和毒品合谋时：引起痤疮样皮肤毒性。

抑制EGFR和MEK的抗肿瘤药的治疗通常受到皮肤不良反应的限制，最常见的是痤疮样爆发。在JCI的这一期中，Satoh等人。定义了痤疮样皮肤毒性的机制，其中EGFR / MEK抑制剂与皮肤共生角质层痤疮共同通过角质素样因子4和NF-κB转录因子在IL-36γ启动子上的联合作用在角质形成细胞中诱导IL-36γ，从而中性粒细胞募集。除了阐明为什么EGFR / MEK抑制剂引起的皮疹经常以脓疱和以卵泡为中心的皮疹外，该机制还为长期采用抗生素治疗的实践提供了依据。