TRIM41 contributes to the pathogenesis of airway allergy by compromising dendritic cells' tolerogenic properties

TRIM41 通过损害树突状细胞的耐受性导致呼吸道过敏的发病机制

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作者:Qiuying Peng, Xiangqian Luo, Lihua Mo, Xuejie Xu, Yu Liu, Dabo Liu, Pingchang Yang

Abstract

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.

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