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Review | Open Access

Basic helix–loop–helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases

Fanglin Shao1,‡ , Zhipeng Wang2,‡, Luxia Ye3,‡, Ruicheng Wu4,‡, Jie Wang4, Qing-Xin Yu5, Dilinaer Wusiman6,7, Zhouting Tuo1,8, Koo Han Yoo9, Ziyu Shu10,11, Wuran Wei4, Dengxiong Li4( ), William C. Cho12( ), Zhihong Liu4( ), Dechao Feng4,13( )
Chengdu Basebio Company, Tianfu Third Street, High-Tech Zone, Chengdu 610041, China
Department of Urology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, First Ring Road, Qingyang District, Chengdu 610041, China
Department of Public Research Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, West Gate Street, Linhai City 317000, Zhejiang Province, China
Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Renmin South Road, Wuhou District, Chengdu 610041, China
Department of Pathology, Ningbo Clinical Pathology Diagnosis Center, Huancheng North Road, Jiangbei District, Ningbo, Zhejiang Province, 315211, China
Department of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, 625 Harrison Street, West Lafayette, IN 47907, USA
Purdue Institute for Cancer Research, Purdue University, 615 W. State Street, West Lafayette, IN 47907, USA
Department of Urology, The Second Affiliated Hospital of Anhui Medical University, Jinzhai South Road, Shushan District, Hefei, Anhui 230032, China
Department of Urology, Kyung Hee University, 26 Kyungheedae-Ro, Dongdaemun-Gu, South Korea
Department of Earth Science and Engineering, Imperial College London, Exhibition Road, South Kensington, London SW7 2AZ, UK
Joint International Research Laboratory of Green Buildings and Built Environments (Ministry of Education), Chongqing University, Shapingba Street, Shapingba District, Chongqing 400044, China
Department of Clinical Oncology, Queen Elizabeth Hospital, Gascoigne Road, Yau Ma Tei, Kowloon, Hong Kong SAR, China
Division of Surgery & Interventional Science, University College London, Gower Street, London W1T 6JF, London W1W 7TS, UK

‡Fanglin Shao, Zhipeng Wang, Luxia Ye, and Ruicheng Wu contributed equally to this work.

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Abstract

The circadian clock is an internal timekeeper system that regulates biological processes through a central circadian clock and peripheral clocks controlling various genes. Basic helix–loop–helix ARNT-like 1 (BMAL1), also known as aryl hydrocarbon receptor nuclear translocator-like protein 1 (ARNTL1), is a key component of the circadian clock. The deletion of BMAL1 alone can abolish the circadian rhythms of the human body. BMAL1 plays a critical role in immune cell function. Dysregulation of BMAL1 is linked to immune-related diseases such as autoimmune diseases, infectious diseases, and cancer, and vice versa. This review highlights the significant role of BMAL1 in governing immune cells, including their development, differentiation, migration, homing, metabolism, and effector functions. This study also explores how dysregulation of BMAL1 can have far-reaching implications and potentially contribute to the onset of immune-related diseases such as autoimmune diseases, infectious diseases, cancer, sepsis, and trauma. Furthermore, this review discusses treatments for immune-related diseases that target BMAL1 disorders. Understanding the impact of BMAL1 on immune function can provide insights into the pathogenesis of immune-related diseases and help in the development of more effective treatment strategies. Targeting BMAL1 has been demonstrated to achieve good efficacy in immune-related diseases, indicating its promising potential as a targetable therapeutic target in these diseases.

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Burns & Trauma
Article number: tkae075

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Cite this article:
Shao F, Wang Z, Ye L, et al. Basic helix–loop–helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases. Burns & Trauma, 2025, 13(2): tkae075. https://doi.org/10.1093/burnst/tkae075

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Received: 06 July 2024
Revised: 26 October 2024
Accepted: 01 November 2024
Published: 10 October 2026
© The Author(s) 2025. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com