AHR: Making the Keratinocytes Thick Skinned

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AHR: Making the Keratinocytes Thick Skinned Marco Colonna  Immunity  Volume 40, Issue 6, Pages 863-864 (June 2014) DOI: 10.1016/j.immuni.2014.06.001 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 AhR Regulation of Keratinocytes At the epidermal surface, UV light and/or resident microorganisms produce tryptophan and idole breakdown products, including FICZ. These polyaromatic hydrocarbons are ligands for the transcription factor AhR in keratinocytes, and their binding causes translocation to the nucleus and subsequent transcriptional changes. In this way, AhR helps reduce keratinocyte responses to cytokines such as IL-1β, leading to decreased transcription of the AP-1 family member Jun-B, a transcription factor previously implicated in psoriasis and keratinocyte proliferation. This ultimately results in decreased psoriatic pathology in AhR-competent compared to AhR-deficient skin. Abbreviations are as follows: T = T cell; ILC = innate lymphoid cell. Immunity 2014 40, 863-864DOI: (10.1016/j.immuni.2014.06.001) Copyright © 2014 Elsevier Inc. Terms and Conditions