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Review Article | Open Access

The implication of dendritic cells in lung diseases: Immunological role of toll-like receptor 4

Shurui Xuana,b,1Yuan Maa,1Honglei ZhoucShengwei GuaXin Yaoa( )Xiaoning Zenga( )
Department of Pulmonary & Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China
Department of Respiratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, China
Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China

1 These authors contributed equally to this work.

Peer review under responsibility of Chongqing Medical University.

Show Author Information

Abstract

The immune responses play a profound role in the progression of lung lesions in both infectious and non-infectious diseases. Dendritic cells, as the “frontline” immune cells responsible for antigen presentation, set up a bridge between innate and adaptive immunity in the course of these diseases. Among the receptors equipped in dendritic cells, Toll-like receptors are a group of specialized receptors as one type of pattern recognition receptors, capable of sensing environmental signals including invading pathogens and self-antigens. Toll-like receptor 4, a pivotal member of the Toll-like receptor family, was formerly recognized as a receptor sensitive to the outer membrane component lipopolysaccharide derived from Gram-negative bacteria, triggering the subsequent response. Moreover, its other essential roles in immune responses have drawn significant attention in the past decade. A better understanding of the implication of Toll-like receptor 4 in dendritic cells could contribute to the management of pulmonary diseases including pneumonia, pulmonary tuberculosis, asthma, acute lung injury, and lung cancer.

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Genes & Diseases
Article number: 101007
Cite this article:
Xuan S, Ma Y, Zhou H, et al. The implication of dendritic cells in lung diseases: Immunological role of toll-like receptor 4. Genes & Diseases, 2024, 11(6): 101007. https://doi.org/10.1016/j.gendis.2023.04.036

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Received: 04 February 2023
Revised: 11 April 2023
Accepted: 17 April 2023
Published: 27 June 2023
© 2023 The Authors.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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