Oncotarget

Research Papers:

Impaired epidermal Langerhans cell maturation in TGFβ-inducible early gene 1 (TIEG1) knockout mice

Xilin Zhang, Yi Yao, Wei-Zen Wei, Zeng-Quan Yang, Jun Gu and Li Zhou _

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Oncotarget. 2017; 8:112875-112882. https://doi.org/10.18632/oncotarget.22843

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Abstract

Xilin Zhang1,3, Yi Yao1,2, Wei-Zen Wei4, Zeng-Quan Yang4, Jun Gu3 and Li Zhou1,2,5

1Center for Cutaneous Biology and Immunology Research, Department of Dermatology, Henry Ford Health System, Detroit, MI, USA

2Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health System, Detroit, MI, USA

3Department of Dermatology, Second Military Medical University Changhai Hospital, Shanghai, China

4Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA

5Department of Internal Medicine, Henry Ford Health System, Detroit, MI, USA

Correspondence to:

Li Zhou, email: lzhou1@hfhs.org

Jun Gu, email: gujun79@163.com

Keywords: Langerhans cell; TIEG1; maturation; TGF-β1 signaling

Received: May 30, 2017    Accepted: November 11, 2017    Published: December 01, 2017

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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