Tolerogenic dendritic cells and TLR4/IRAK4/NF-κB signaling pathway in allergic rhinitis

Chenglin Kang; Xiaomei Li; Peng Liu; Yue Liu; Yuan Niu; Xianhai Zeng; Hailiang Zhao; Jiangqi Liu; Shuqi Qiu

doi:10.3389/fimmu.2023.1276512

Tolerogenic dendritic cells and TLR4/IRAK4/NF-κB signaling pathway in allergic rhinitis

Front Immunol. 2023 Oct 17:14:1276512. doi: 10.3389/fimmu.2023.1276512. eCollection 2023.

Authors

Chenglin Kang^{1

2

3}, Xiaomei Li³, Peng Liu¹, Yue Liu¹, Yuan Niu⁴, Xianhai Zeng^{1

2}, Hailiang Zhao^{1

2}, Jiangqi Liu^{1

2}, Shuqi Qiu^{1

2}

Affiliations

¹ Department of Graduate and Scientific Research, Zunyi Medical University Zhuhai Campus, Zhuhai, China.
² Department of Otolaryngology, Longgang E.N.T Hospital and Shenzhen Key Laboratory of E.N.T, Institute of E.N.T Shenzhen, Shenzhen, China.
³ Department of Otolaryngology, Second People's Hospital of Gansu Province, Lanzhou, China.
⁴ Department of Neurology, Second People's Hospital of Gansu Province, Lanzhou, China.

Abstract

Dendritic cells (DCs), central participants in the allergic immune response, can capture and present allergens leading to allergic inflammation in the immunopathogenesis of allergic rhinitis (AR). In addition to initiating antigen-specific immune responses, DCs induce tolerance and modulate immune homeostasis. As a special type of DCs, tolerogenic DCs (tolDCs) achieve immune tolerance mainly by suppressing effector T cell responses and inducing regulatory T cells (Tregs). TolDCs suppress allergic inflammation by modulating immune tolerance, thereby reducing symptoms of AR. Activation of the TLR4/IRAK4/NF-κB signaling pathway contributes to the release of inflammatory cytokines, and inhibitors of this signaling pathway induce the production of tolDCs to alleviate allergic inflammatory responses. This review focuses on the relationship between tolDCs and TLR4/IRAK4/NF-κB signaling pathway with AR.

Keywords: TLR4/IRAK4/NF-κB signaling pathway; allergic rhinitis; immune response; immune tolerance; tolerogenic dendritic cells.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Dendritic Cells
Humans
Inflammation
Interleukin-1 Receptor-Associated Kinases
NF-kappa B*
Rhinitis, Allergic*
Signal Transduction
Toll-Like Receptor 4

Substances

NF-kappa B
Toll-Like Receptor 4
Interleukin-1 Receptor-Associated Kinases
TLR4 protein, human
IRAK4 protein, human

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants Natural Science Foundation of China (No. 81700888), Guangdong Basic and Applied Basic Research Foundation (No. 2021A1515010971), Shenzhen Science and Technology Program for Basic Research (No. JCYJ20220531091417040), Shenzhen Science and Technology Program (No. JCYJ20210324142207019), Shenzhen Key Medical Discipline Construction Fund (No. SZXK039), Science and Technology Development Special Fund of Shenzhen Longgang District (No. LGKCYLWS2019000864, LGKCZSYS2019000046), Science and Technology Innovation Special-Technology Tackling Project of Shenzhen Longgang District (No. LGKCYLWS2022032).