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已发表论文

嗜碱性粒细胞在特应性皮炎中的作用:从发病机制到治疗展望

 

Authors Wang P, Su Z, Sun C , Yao WH, Zeng YP 

Received 12 February 2025

Accepted for publication 23 April 2025

Published 2 May 2025 Volume 2025:18 Pages 675—682

DOI http://doi.org/10.2147/JAA.S522343

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Luis Garcia-Marcos

Pan Wang,1,2 Zheng Su,2 Chen Sun,2 Wen-Hui Yao,2 Yue-Ping Zeng2 

1School of Medicine, Sun Yat-Sen University, Shenzhen, People’s Republic of China; 2Department of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, People’s Republic of China

Correspondence: Yue-Ping Zeng, Department of Dermatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1, Shuaifuyuan, Dongcheng District, Beijing, 100730, People’s Republic of China, Email zengyueping0917@126.com

Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by intense pruritus. The principal pathological features include abnormalities in the structure and function of the epidermis, as well as skin inflammation marked by the overexpression of T helper 2 cell (Th2) cytokines. Throughout the progression of AD, various immune cells contribute to its pathogenesis. Basophils, the least abundant granulocytes in the human peripheral circulation, have historically been overlooked. However, the advent of novel research tools has facilitated a renewed focus on the role of basophils in diverse physiological and pathological conditions, including AD. Accordingly, this review will primarily summarize the association between AD and basophils, the alterations observed in basophils among AD patients, and the implications of these changes for AD patients.

Keywords: basophils, atopic dermatitis, AD, Th2 inflammation, synergistic interactions

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