TGF-β-inducible early gene 1 (TIEG1), also known as Krüppel-like factor 10 (Klf10), represents a major downstream transcription factor of transforming growth factor-β1 (TGF-β1) signaling. Epidermal Langerhans cells (LCs), a unique subpopulation of dendritic cells (DC), essentially mediates immune surveillance and tolerance. TGF-β1 plays a pivotal role in LC maintenance and function after birth, although the underpinning mechanisms remain elusive. Here, we hypothesized that TIEG1 might be involved in TGF-β1-mediated LC homeostasis and function. Utilizing TIEG1 null mice, we discovered that TIEG1 deficiency did not alter LC homeostasis at the steady state and LC repopulation at inflamed-state, as well as their antigen-uptake capacity, but significantly impaired their maturation ability, which was opposite to the fact that loss of TGF-β1 induced spontaneous LC maturation. Moreover, the ablation of TIEG1 enhanced skin contact hypersensitivity response. Our results suggested that TIEG1 is not a key molecule involved in TGF-β1-mediated homeostasis, while TIEG1-related signaling pathways regulate LC maturation and their function.