Langerhans cells (LCs), a subpopulation of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and MAPK and mTOR activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling-regulated kinase (ERK) and the mammalian target of rapamycin (mTOR) cascade. In previous work we demonstrated, that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In the current study we extended our analysis on p14-deficiency specifically in LCs. Langerin-specific ablation of p14 caused a complete loss of LCs, accompanied by an increased maturational phenotype of LCs. The absence of LCs in p14-deficient mice reduced contact hypersensitivity responses to the contact sensitizer TNCB. Analysis using bone marrow-derived DCs (BMDCs) revealed, that p14 deficiency in DCs/LCs interfered with the LC-relevant TGFß1 pathway, by lowering TGFß receptor II expression on BMDCs and LCs as well as surface-binding of TGFß1 on BMDCs. We conclude, that p14-deficiency affects TGFß1 sensitivity of LCs, which is mandatory for their homeostasis and subsequently for their immunological function during contact hypersensitivity.Journal of Investigative Dermatology accepted article preview online, 31 July 2014; doi:10.1038/jid.2014.324.