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Langerhans cells (LCs) are skin-homing dendritic cells (DCs) that have long been considered to be prototypic sentinel DCs due to their prominent position at the environmental barrier, and are essential for the induction of skin immunity and tolerance [1]. Transforming growth factor-β1 (TGF-β1) is a key factor in epidermal LC development and maintenance. The presence of TGF-β1 is a prerequisite for in vitro LC differentiation from various sources. For examples, human CD34+ hematopoietic progenitor cells expanded and developed into LCs in a stringent TGF-β1-dependent manner under serum-free conditions. Both TGF-β1 and TGF-β receptor II (TGF- βRII) null mice exhibited a profound LC loss in skin [2]. Furthermore, LCs are absent in mice that lack Id2 and Runx3, the transcription factors controlled by the TGF-β pathways. In the DC-specific TGF-βRI knockout (KO) mice, LCs disappeared within the first week after birth and displayed increased expressions of costimulatory and pro-motility molecules, suggesting that TGF-β1 is also required to maintain the immature status of epidermal LCs [3]. Latest studies also suggested that TGF-β1 inhibits steady-state and inflammation-induced LCs maturation and migration [4].

TGF-β1-Smad signaling pathways are not required for epidermal LC homeostasis