Loss of MicroRNA29 expression in B cells and skin microbiota synergize to promote atopic dermatitis in mice 2581 Article Swipe

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Timothy C. Borbet , Marcus J. Hines , Kimberly S Zaldana , Marianna Shvartsbeyn , Tate Morrison , Thomas Boehringer , Briana J. Mullins , Sandra González , Sofia Bajwa , Sergei B. Koralov ·

YOU? · · 2025 · Open Access · · DOI: https://doi.org/10.1093/jimmun/vkaf283.485

Description Our research focuses on the role of the microRNA(miR)29 family to regulate peripheral B cell survival and function. We hypothesized that mice with miR29-deficient B cells (B29KO) would have reduced B cell survival and heightened autoreactive B cell receptors (BCRs). Our investigations using B29KO mice revealed a novel target transcript, Il4ra. B29KO mice develop itching and skin inflammation, with a 50% mortality rate. We found B29KO B cells have higher expression of Il4ra by both qPCR and single-cell sequencing. Differential gene analysis and pathway enrichment show, relative to littermate controls, miR29-deficient B cells exhibit heightened IL4 signaling, reduced activation, and negative regulation of cytokine production. When B29KO B cells are stimulated with IL-4 and anti-CD40 ex vivo, they exhibit greater class switching to IgE than wild-type B cells, a finding recapitulated in B29KO mice that have higher serum IgE titers. To rescue the phenotype, B29KO mice were treated with a neutralizing anti-IL4Ra antibody fully rescued the mice from mortality, confirming the importance of IL-4 signaling to this phenotype. We found that skin swabs from phenotypic B29KO mice transferred the phenotype to healthy B29KO mice but not littermate controls. Donor and recipient mice were found to be colonized with Staphylococcus aureus and xylosus. This work supports a role for miR29 in regulating susceptibility to atopic dermatitis in mice via genetic susceptibility and microbial triggers. Funding Sources NIAID 3R43AI136141, BSF, Bernard Levine Fellowship Topic Categories Immediate Hypersensitivity, Asthma, and Allergic Responses (HYP)

Related Topics

Immunoglobulin Class Switching

Immune System

Staphylococcus Aureus

Concepts

Immunology Immunoglobulin E Atopic dermatitis Phenotype Biology Antibody Cytokine Interleukin 4 B cell Receptor Immunoglobulin class switching Immune system Staphylococcus aureus Ratón Scratching Interleukin 10 clone (Java method) T cell Downregulation and upregulation Cell Signal transduction Allergy Medicine Gene Interleukin Mast cell CD40 Cell culture Interleukin 5

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Type: article
Language: en
Landing Page: https://doi.org/10.1093/jimmun/vkaf283.485
PDF: https://academic.oup.com/jimmunol/article-pdf/214/Supplement_1/vkaf283.485/65411346/vkaf283.485.pdf
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DOI: https://doi.org/10.1093/jimmun/vkaf283.485

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Title: Loss of MicroRNA29 expression in B cells and skin microbiota synergize to promote atopic dermatitis in mice 2581

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Language: en

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Publication year: 2025

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Publication date: 2025-11-01

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Authors: Timothy C. Borbet, Marcus J. Hines, Kimberly S Zaldana, Marianna Shvartsbeyn, Tate Morrison, Thomas Boehringer, Briana J. Mullins, Sandra González, Sofia Bajwa, Sergei B. Koralov

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Landing page: https://doi.org/10.1093/jimmun/vkaf283.485

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Concepts: Immunology, Immunoglobulin E, Atopic dermatitis, Phenotype, Biology, Antibody, Cytokine, Interleukin 4, B cell, Receptor, Immunoglobulin class switching, Immune system, Staphylococcus aureus, Ratón, Scratching, Interleukin 10, clone (Java method), T cell, Downregulation and upregulation, Cell, Signal transduction, Allergy, Medicine, Gene, Interleukin, Mast cell, CD40, Cell culture, Interleukin 5

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primary_location.license_id
primary_location.is_accepted	True
primary_location.is_published	True
primary_location.raw_source_name	The Journal of Immunology
primary_location.landing_page_url	https://doi.org/10.1093/jimmun/vkaf283.485
publication_date	2025-11-01
publication_year	2025
referenced_works_count	0
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abstract_inverted_index.a	48, 61, 130, 151, 207
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abstract_inverted_index.by	75
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abstract_inverted_index.on	5
abstract_inverted_index.to	12, 89, 124, 167, 182, 196, 214
abstract_inverted_index.50%	62
abstract_inverted_index.IL4	97
abstract_inverted_index.IgE	125, 140
abstract_inverted_index.Our	2, 42
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abstract_inverted_index.BSF,	229
abstract_inverted_index.IL-4	114, 165
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abstract_inverted_index.qPCR	77
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abstract_inverted_index.(HYP)	241
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abstract_inverted_index.Donor	190
abstract_inverted_index.Il4ra	74
abstract_inverted_index.NIAID	227
abstract_inverted_index.Topic	233
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abstract_inverted_index.miR29	210
abstract_inverted_index.novel	49
abstract_inverted_index.rate.	64
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abstract_inverted_index.show,	87
abstract_inverted_index.swabs	174
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abstract_inverted_index.Levine	231
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abstract_inverted_index.aureus	201
abstract_inverted_index.cells,	129
abstract_inverted_index.family	11
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abstract_inverted_index.target	50
abstract_inverted_index.(B29KO)	28
abstract_inverted_index.(BCRs).	41
abstract_inverted_index.Asthma,	237
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abstract_inverted_index.Funding	225
abstract_inverted_index.Sources	226
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abstract_inverted_index.negative	102
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abstract_inverted_index.xylosus.	203
abstract_inverted_index.Immediate	235
abstract_inverted_index.Responses	240
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abstract_inverted_index.controls,	91
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abstract_inverted_index.receptors	40
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abstract_inverted_index.dermatitis	216
abstract_inverted_index.enrichment	86
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abstract_inverted_index.phenotype,	145
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abstract_inverted_index.single-cell	79
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abstract_inverted_index.investigations	43
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