Abstract
Transforming growth factor-β1 (TGFβ1) is generally regarded as an anti-inflammatory cytokine. However, previous studies suggest that TGFβ1 can promote immune responses under certain conditions. In this issue, Mohammed et al. report that epidermal keratinocyte-derived TGFβ1 alone can alter homeostasis of multiple cutaneous dendritic cell (DC) subsets, which may enhance skin inflammation. These findings may provide a better understanding of the pathogenesis of inflammatory skin disorders such as psoriasis, although how keratinocyte-derived TGFβ1 regulates cutaneous DCs under physiological and inflammatory conditions should be further addressed.
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