TXNIP regulates natural killer cell-mediated innate immunity by inhibiting IFN-γ production during bacterial infection

Cited 1 time in scopus
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Title
TXNIP regulates natural killer cell-mediated innate immunity by inhibiting IFN-γ production during bacterial infection
Author(s)
D O Kim; Jae Eun Byun; Won Sam Kim; M J Kim; Jung Ha Choi; Hanna Kim; Eunji Choi; Tae-Don KimSuk Ran YoonJi Yoon NohYoung-Jun ParkJungwoon LeeHee Jun ChoHee Gu Lee; S H Min; Inpyo ChoiHaiyoung Jung
Bibliographic Citation
International Journal of Molecular Sciences, vol. 21, no. 24, pp. 9499-9499
Publication Year
2020
Abstract
The function of natural killer (NK) cell-derived interferon-γ (IFN-γ) expands to remove pathogens by increasing the ability of innate immune cells. Here, we identified the critical role of thioredoxin-interacting protein (TXNIP) in the production of IFN-γ in NK cells during bacterial infection. TXNIP inhibited the production of IFN-γ and the activation of transforming growth factor β-activated kinase 1 (TAK1) activity in primary mouse and human NK cells. TXNIP directly interacted with TAK1 and inhibited TAK1 activity by interfering with the complex formation between TAK1 and TAK1 binding protein 1 (TAB1). Txnip?/? (KO) NK cells enhanced the activation of macrophages by inducing IFN-γ production during Pam3CSK4 stimulation or Staphylococcus aureus (S. aureus) infection and contributed to expedite the bacterial clearance. Our findings suggest that NK cell-derived IFN-γ is critical for host defense and that TXNIP plays an important role as an inhibitor of NK cell-mediated macrophage activation by inhibiting the production of IFN-γ during bacterial infection.
Keyword
NK cellIFN-γTXNIPTAK1Toll-like receptor (TLR)Bacterial infection
ISSN
1661-6596
Publisher
MDPI
DOI
http://dx.doi.org/10.3390/ijms21249499
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
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