NFATc1 deficiency in B cells ameliorates atopic dermatitis

NFATc1 deficiency in B cells ameliorates atopic dermatitis

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 a...

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Main Authors: Hidaya Abdul Kader, Syed Sabih Ur Rehman, Dhanya Saraswathiamma, Sadiya Sadiq Shiek, Antonio A. Bencomo-Hernández, Ubaid Rahman Moorakkan, Muhammad Touseef Haider, Nayla Munawar, Rabah Iratni, Edgar Serfling, Mohammad Tauqeer Alam, Khalid Muhammad
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Scientific Reports
Subjects:
Atopic dermatitis (AD)
Regulatory B cells (Bregs)
IL-10
NFATc1
IgE
Online Access:https://doi.org/10.1038/s41598-025-11247-9
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Summary: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 f/f x mb1cre AD mice exhibited a diminished AD phenotype compared with WT AD mice, by reduced ear swelling, lower epidermal thickening, and fewer cellular infiltration to ear. This was evident by unaltered IgE levels. Interestingly, Nfatc1 f/f xmb1cre AD mice displayed a higher percentage of IL-10-producing B220+CD5+CD1d+ Breg cells, indicating that NFATc1 deficiency promotes the differentiation of B cells into Bregs that produce more anti-inflammatory IL-10, thus alleviating AD symptoms. At the transcriptome level, NFATc1 deficient B cells bearing AD mice exhibited distinct gene expression profiles compared with WT AD mice, with genes that promoted B-cell development and enhanced stress and stimulus responses. This study highlights the potential of targeting NFATc1 as a molecular strategy to reduce AD symptoms without impairing B-cell function while boosting the production of the endogenous anti-inflammatory IL-10.
ISSN:2045-2322

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