TRIM41 contributes to the pathogenesis of airway allergy by compromising dendritic cells’ tolerogenic properties
Qiuying Peng,
Xiangqian Luo,
Lihua Mo,
Xuejie Xu,
Yu Liu,
Dabo Liu,
Pingchang Yang
Affiliations
Qiuying Peng
Department of Pediatric Otolaryngology, Shenzhen Hospital of Southern Medical University, Shenzhen, China; Department of Pediatrics, Guangzhou Panyu Maternal and Children Health Hospital, Guangzhou, China
Xiangqian Luo
Department of Pediatric Otolaryngology, Shenzhen Hospital of Southern Medical University, Shenzhen, China
Lihua Mo
Department of Pediatric Otolaryngology, Shenzhen Hospital of Southern Medical University, Shenzhen, China; Institute of Allergy & Immunology of Shenzhen University and State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China; Department of General Practice Medicine, Third Affiliated Hospital of Shenzhen University, Shenzhen, China
Xuejie Xu
Institute of Allergy & Immunology of Shenzhen University and State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China
Yu Liu
Department of General Practice Medicine, Third Affiliated Hospital of Shenzhen University, Shenzhen, China
Dabo Liu
Department of Pediatric Otolaryngology, Shenzhen Hospital of Southern Medical University, Shenzhen, China; Corresponding author
Pingchang Yang
Institute of Allergy & Immunology of Shenzhen University and State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China; Corresponding author
Summary: Dendritic cells (DC) play a crucial role in the initiation of immune responses. TRIM41, an E3 ubiquitin ligase, can facilitate targeting protein degradation. The purpose of this study is to analyze the role of TRIM41 in the pathogenesis of airway allergy (AA) and the impact of regulating TRIM41 on suppressing AA. We observed that the airway DCs of AA mice had a higher expression of Trim41. The expression of Trim41 in airway DCs was associated with the DCs’ tolerogenic functions of AA mice. The AA responses, including increased amounts of eosinophil peroxidase, mast cell protease-1, Th2 cytokines, and specific IgE in bronchoalveolar lavage fluids, were positively correlated with the Trim41 expression in mouse airway DCs. TRIM41 induced c-Maf degradation and interfered with the Il10 expression in airway DCs, which could be counteracted by inhibiting TRIM41. Regulation of TRIM41 mitigated experimental AA responses.
