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<p>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 <i>Nfatc1</i><sup><i>f/f</i></sup> <i>x mb1cre</i> 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, <i>Nfatc1</i><sup><i>f/f</i></sup><i>xmb1cre</i> AD mice displayed a higher percentage of IL-10-producing B220<sup>+</sup>CD5<sup>+</sup>CD1d<sup>+</sup> 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.</p>

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NFATc1 deficiency in B cells ameliorates atopic dermatitis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月11日

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  • 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

摘要

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 Nfatc1f/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, Nfatc1f/fxmb1cre 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.