ArticleInternational archives of allergy and immunology
Lack of WDFY4 Aggravates Ovalbumin-Induced Asthma via Enhanced Th2 Cell Differentiation.
Article in International archives of allergy and immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Epigenetic alterations in WDFY4 DNA methylation are linked to immunoinflammatory processes in rheumatoid arthritis: insights from a case-control study.Clinical rheumatology · 2026Article
- WDFY4 Promotes the Progression of Atherosclerosis by Regulating Ferroptosis Mediated by the LAPTM5/CDC42/mTOR/4EBP1/SLC7A11 Pathway.Journal of cellular and molecular medicine · 2025Article
- Lack of WDFY4 leads to impaired immune response and poor cancer prognosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Analysis of WDFY4 rs7097397 and PHLDB1 rs7389 polymorphisms in Chinese patients with systemic lupus erythematosus.Clinical rheumatology · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthma is a chronic inflammatory airway disease, and Th2 cells play an important role in asthma. WDFY4 (WDFY family member 4) is a susceptibility gene in several autoimmune diseases.
objectiveIn this study, the roles of WDFY4 in Th2 cell differentiation and Th2-dependent asthma were investigated.
methodsNaïve CD4+ T cells were isolated from wild-type and WDFY4-deficient mice and induced to differentiate in vitro. Subsequently, a mouse model of asthma was established by sensitization with ovalbumin.
resultsStudy results showed that WDFY4 deficiency could promote the differentiation of Th2 cells and the production of Th2 cytokines. WDFY4-deficient asthmatic mice showed higher levels of Th2 cytokines in the lungs and bronchoalveolar lavage fluid than wild-type mice. Moreover, infiltration of inflammatory cells, hyperplasia of goblet cells, production of mucus, and deposition of collagen were enhanced in WDFY4-deficient asthmatic mice.
conclusionsOur study demonstrates the pivotal role of WDFY4 in the pathogenesis of asthma and in Th2 cell differentiation.
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