ArticleScientific reports2025
NFATc1 deficiency in B cells ameliorates atopic dermatitis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Building an Interleukin-10-Producing Identity: How B Cells Acquire Interleukin-10 Competence and How Plasma Cell Differentiation Consolidates This Program.Immunological reviews · 2026Review
- Nuclear factor of activated T cells as a driver of tumor progression and a target for precision therapy.Animal models and experimental medicine · 2026Review
- Integrative Transcriptomic, Network, and Genomic Analysis of Peripheral Blood Mononuclear Cells Identifies Candidate Genes Associated with Dupilumab Clinical Response in Atopic Dermatitis Patients.International journal of molecular sciences · 2026Article
- Influence and Role of Regulatory B Cells in Organ Transplantation: The State of the Art, Prospects, and Emerging Insights.Antibodies (Basel, Switzerland) · 2025Review
- Pentanoate modulates B cells to suppress allergic contact hypersensitivity.Scientific reports · 2025Article
- NFATc1 Abrogation in B Cells Ameliorates Contact Hypersensitivity Responses.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic dermatitis (AD) is a common skin allergy, affecting large population worldwide. Currently, there is no cure for AD. NFATc1, a transcription factor, operates through a calcium-dependent calcineurin/calmodulin pathway to regulate target genes and is vital in immune system development and function. Previous research suggests that NFATc1 suppresses IL-10 in B cells by binding to its gene. Our current study explores the role of B cells deficient of NFATc1 during calcipotriol, a vitamin D analog, induced AD responses. Our data showed that Nfatc1
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Registered trials
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