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NFATc1 deficiency in B cells ameliorates atopic dermatitis
Hidaya Abdul Kader1, Syed Sabih Ur Rehman1, Dhanya Saraswathiamma2
1Department of Biology, College of Science, United Arab Emirates University, 15551, Al Ain, United Arab Emirates.
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 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.
Insights
Targeting NFATc1 in B cells reduces atopic dermatitis (AD) symptoms by increasing anti-inflammatory IL-10. This approach alleviates skin inflammation without impairing B-cell function, offering a novel therapeutic strategy for AD.
Area of Science:
- Immunology
- Dermatology
- Molecular Biology
Background:
- Atopic dermatitis (AD) is a prevalent global skin condition with no current cure.
- NFATc1 is a transcription factor crucial for immune function, known to suppress IL-10 in B cells.
- Understanding NFATc1's role in B cells is key to developing new AD treatments.
Purpose of the Study:
- To investigate the role of NFATc1-deficient B cells in a mouse model of atopic dermatitis.
- To determine if NFATc1 deficiency impacts AD phenotype and IL-10 production in B cells.
- To explore the transcriptomic changes in NFATc1-deficient B cells during AD.
Main Methods:
- Utilized Nfatc1-deficient (Nfatc1f/f x mb1cre) and wild-type (WT) AD mouse models.
- Administered calcipotriol to induce AD-like skin inflammation.
- Analyzed AD phenotype (ear swelling, epidermal thickness, cellular infiltration), IgE levels, B cell populations (Bregs), IL-10 production, and gene expression profiles.
Main Results:
- Nfatc1f/f x mb1cre AD mice showed significantly reduced AD symptoms compared to WT AD mice.
- NFATc1 deficiency in B cells led to an increased percentage of IL-10-producing B cells (Bregs).
- Transcriptome analysis revealed distinct gene expression patterns in NFATc1-deficient B cells, favoring B-cell development and stress responses.
Conclusions:
- NFATc1 deficiency in B cells promotes the differentiation of IL-10-producing Bregs, effectively alleviating AD symptoms.
- Targeting NFATc1 presents a potential therapeutic strategy for AD, enhancing anti-inflammatory IL-10 production without compromising B-cell function.
- This study highlights the intricate role of NFATc1 in regulating B-cell responses and its therapeutic potential in atopic dermatitis.
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