Bintao Su, Quanhong Zhang, Xianyong Hu, Bo Xie, Chao Chen, Yan Zhao, Zhi Liu, Ling Ma, Jinbo Chen
{"title":"Role of basophils and type 2 inflammation in bullous pemphigoid pathophysiology: a comparative study of blood and blister fluid.","authors":"Bintao Su, Quanhong Zhang, Xianyong Hu, Bo Xie, Chao Chen, Yan Zhao, Zhi Liu, Ling Ma, Jinbo Chen","doi":"10.1007/s12026-025-09617-6","DOIUrl":null,"url":null,"abstract":"<p><p>Bullous pemphigoid (BP) is an autoimmune disease characterized by blister formation and inflammatory cell infiltration. In addition to eosinophil and neutrophil infiltration, there are many other inflammatory cells and factors involved in the pathophysiology of BP. Elucidating the inflammation environment will help to the diagnosis and treatment of BP. We used flow cytometry and wright-stained smears to analyze immune cells, and cytometric bead array methods were used to analyze immune factors in matched blood and blister fluid. Besides abundant eosinophil and neutrophil accumulation, distinct basophil infiltration was detected in blister fluid of patients with BP. We also found significant CD4<sup>+</sup> T lymphocyte activation and increased type 2 cytokine secretion in BP blister fluid. Under no stimulation, basophils produce more IL-4 compared to CD4<sup>+</sup> T lymphocytes in BP blister fluid. Basophils might play a more important role in BP than we early thought. Along with other inflammatory cells and factors, basophils, demonstrated as one of the main producers of IL-4, orchestrate the type 2 inflammation environment in BP.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"68"},"PeriodicalIF":3.3000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunologic Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12026-025-09617-6","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Bullous pemphigoid (BP) is an autoimmune disease characterized by blister formation and inflammatory cell infiltration. In addition to eosinophil and neutrophil infiltration, there are many other inflammatory cells and factors involved in the pathophysiology of BP. Elucidating the inflammation environment will help to the diagnosis and treatment of BP. We used flow cytometry and wright-stained smears to analyze immune cells, and cytometric bead array methods were used to analyze immune factors in matched blood and blister fluid. Besides abundant eosinophil and neutrophil accumulation, distinct basophil infiltration was detected in blister fluid of patients with BP. We also found significant CD4+ T lymphocyte activation and increased type 2 cytokine secretion in BP blister fluid. Under no stimulation, basophils produce more IL-4 compared to CD4+ T lymphocytes in BP blister fluid. Basophils might play a more important role in BP than we early thought. Along with other inflammatory cells and factors, basophils, demonstrated as one of the main producers of IL-4, orchestrate the type 2 inflammation environment in BP.
期刊介绍:
IMMUNOLOGIC RESEARCH represents a unique medium for the presentation, interpretation, and clarification of complex scientific data. Information is presented in the form of interpretive synthesis reviews, original research articles, symposia, editorials, and theoretical essays. The scope of coverage extends to cellular immunology, immunogenetics, molecular and structural immunology, immunoregulation and autoimmunity, immunopathology, tumor immunology, host defense and microbial immunity, including viral immunology, immunohematology, mucosal immunity, complement, transplantation immunology, clinical immunology, neuroimmunology, immunoendocrinology, immunotoxicology, translational immunology, and history of immunology.