FOCAL POINT Nguan Soon Tan (center) and colleagues, including lead authors Ming Jie Tan (left) and Han Chung Chong (right) dissect the signals exchanged between fibroblasts and keratinocytes in mammalian skin. Organotypic cultures reveal how the transcription factor PPARβ/δ modulates the fibroblasts’ response to keratinocyte-released IL-1. Fibroblasts lacking either PPARβ/δ or its transcriptional target, sIL-1ra (an inhibitor of IL-1 signaling; right panels), overproduce growth factors that induce the overlying keratinocytes to proliferate excessively (arrows).

FOCAL POINT Nguan Soon Tan (center) and colleagues, including lead authors Ming Jie Tan (left) and Han Chung Chong (right) dissect the signals exchanged between fibroblasts and keratinocytes in mammalian skin. Organotypic cultures reveal how the transcription factor PPARβ/δ modulates the fibroblasts’ response to keratinocyte-released IL-1. Fibroblasts lacking either PPARβ/δ or its transcriptional target, sIL-1ra (an inhibitor of IL-1 signaling; right panels), overproduce growth factors that induce the overlying keratinocytes to proliferate excessively (arrows).

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