ArticleOncotarget2017
Impaired epidermal Langerhans cell maturation in TGFβ-inducible early gene 1 (TIEG1) knockout mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Identification of actionable targets for breast cancer intervention using a diversity outbred mouse model.iScience · 2023Article
- Retinoblastoma cell-derived Twist protein promotes regulatory T cell development.Cancer immunology, immunotherapy : CII · 2021Article
- Smad2/4 Signaling Pathway Is Critical for Epidermal Langerhans Cell Repopulation Under Inflammatory Condition but Not Required for Their Homeostasis at Steady State.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
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