ArticleNature communications2024
Group 2 innate lymphoid cells are a non-redundant source of interleukin-5 required for development and function of murine B1 cells.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- IL-9 Is Essential for ILC2-Mediated but Not Th2- and Th17-Cell-Mediated Allergic Airway Inflammation in Mice.European journal of immunology · 2026Article
- Eosinophil diversity and function: emerging insights into subtypes and therapeutic targets.Cell death discovery · 2026Review
- Blimp-1 integrates alarmin signals in ILC2s and drives proinflammatory functions required for type 2 immunity.The Journal of experimental medicine · 2026Article
- Review
- Distinguishing Features of ILC2s During Type 2 Immune Responses.European journal of immunology · 2026Review
- Advances and mechanisms in the application and treatment of functionalized stem cells and their derivatives in allergic rhinitis.Frontiers in pediatrics · 2026Review
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- Engineered Neuromedin U Promotes Type 2 Innate Immunity and Renoprotection in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Spatial Eosinophil Phenotypes as Immunopathogenic Determinants in Inflammatory Diseases.Cells · 2025Review
- Review
- Unspoken words: decoding the dialog between type 2 innate lymphoid cells and T cells.Frontiers in immunology · 2025Review
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Authors and funding
19 authors.
Funding
Abstract
Tissue-resident immune cells, such as innate lymphoid cells, mediate protective or detrimental immune responses at barrier surfaces. Upon activation by stromal or epithelial cell-derived alarmins, group 2 innate lymphoid cells (ILC2s) are a rapid source of type 2 cytokines, such as IL-5. However, due to the overlap in effector functions, it remains unresolved whether ILC2s are an essential component of the type 2 response or whether their function can be compensated by other cells, such as T cells. Here we show a non-redundant role of ILC2s in supporting the development and function of B1 cells. We demonstrate that B1 cells fail to develop properly in the absence of ILC2s and identify the IL-33 receptor on ILC2s as an essential cell-intrinsic regulator of IL-5 production. Further, conditional deletion of Il5 in ILC2s results in defective B1 cell development and immunoglobulin production. Consequently, B1 cells with phosphatidylcholine specific B cell receptor rearrangements are diminished in ILC2-deficient mice. Thus, our data establish an essential function of ILC2s in supporting B1 cells and antibody production at barrier surfaces.
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