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Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

ABSTRACT: Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

PROVIDER: PRJNA1217864 | ENA |

REPOSITORIES: ENA

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Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

Project description:Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

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Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

Project description:We used single cell RNA sequencing to examine the transcriptome and B cell receptor (BCR) sequences of B cells infiltrating mouse lungs 3 weeks after allergen inhalation to investigate the origins of IgE-producing plasma cells.

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Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

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IgE-binding monocytes upregulate the coagulation cascade in allergic horses

Project description:IgE-binding monocytes are a rare peripheral immune cell type involved in the allergic response through binding of IgE on their surface. IgE-binding monocytes are present in both healthy and allergic individuals. We performed RNA sequencing to ask how the function of IgE-binding monocytes differs in the context of allergy. Using a large animal model of allergy, equine Culicoides hypersensitivity, we compared the transcriptome of IgE-binding monocytes in allergic and non-allergic horses at two seasonal timepoints: (i) when allergic animals were clinical healthy, in the winter “Remission Phase”, and (ii) during chronic disease, in the summer “Clinical Phase”. Most transcriptional differences between allergic and non-allergic horses occurred only during the “Remission Phase”, suggesting principal differences in monocyte function even in the absence of allergen exposure. F13A1, a subunit of fibrinoligase, was significantly upregulated at both timepoints in allergic horses. This suggested a role for increased fibrin deposition in the coagulation cascade to promote allergic inflammation. IgE-binding monocytes also downregulated CCR10 expression in allergic horses during the “Clinical Phase”, suggesting a defect in maintenance of skin homeostasis, which further promotes allergic inflammation. Together, this transcriptional analysis provides valuable clues into the mechanisms used by IgE-binding monocytes in allergic individuals.

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Bulk RNA-sequence of four monocyte-macrophage subpopulations isolated from the IgE-dependent skin allergic inflammation (IgE-CAI) skin lesion

Project description:Basophils play critical roles in the development of mouse delayed-onset skin allergic inflammation (IgE-CAI model). Importantly, they also contribute to the resolution of allergic inflammation by promoting the generation of pro-resolving macrophages. However, it remains unclear how pro-resolving macrophages suppress excess inflammation. To address this, we conducted single-cell RNA-seq (scRNA-seq) analysis of the IgE-CAI skin lesion at days 3 and 5 post-challenge of allergens. scRNA-seq analysis identified four distinct monocyte-macrophage subpopulations, namely classical monoytes, early CMDMs, late CMDMs and resident-like macrophages. Based on the gene expression profiles, classical monoytes, early CMDMs, late CMDMs and resident-like macrophages corresponded to Ly6ChiPD-L2lo, Ly6ChiPD-L2hi, Ly6CloPD-L2hi, and Ly6CloPD-L2lo, respectively.

2024-01-22 | GSE245865 | GEO

Single-cell RNA-sequence of the skin lesion of IgE-dependent skin allergic inflammation (IgE-CAI) model

Project description:Basophils play critical roles in the development of mouse delayed-onset skin allergic inflammation (IgE-CAI model). Importantly, they also contribute to the resolution of allergic inflammation by promoting the generation of pro-resolving macrophages. However, it remains unclear how pro-resolving macrophages suppress excess inflammation. To address this, we conducted single-cell RNA-seq (scRNA-seq) analysis of the IgE-CAI skin lesion at days 3 and 5 post-challenge of allergens. scRNA-seq analysis identified two distinct classical monocyte-derived macrophage (CMDM) populations, namely early and late CMDMs, in IgE-CAI skin lesion. The former population was preferentially observed at the peak of inflammation (day 3), whereas the latter one at the termination phase of inflammation (day 5). Gene ontology analysis revealed that genes associated with phagocytosis were enriched in late CMDMs. In particular, late CMDMs displayed upregulated expression of Gas6 and Mertk, key genes for phagocytic clearance of apoptotic cells. Taken together, scRNA-seq identified CMDMs that display high capacity of dead cell clearance and contribute to the resolution of IgE-CAI.

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Project description:Allergic microbial signature in IgE-mediated food allergies

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Type 2-polarized memory B cells hold allergen-specific IgE memory

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Chronic allergen exposure drives accumulation of long-lived IgE plasma cells in the bone marrow, giving rise to serological memory

Project description:Summary: Long-lived IgE plasma cells reside in the bone marrow of allergic mice and atopic humans, confer IgE serological memory and produce allergen-specific IgE that can drive anaphylaxis. Abstract: Immunoglobulin E (IgE) plays an important role in allergic diseases. Nevertheless, the source of IgE serological memory remains controversial. We re-examined the mechanism of serological memory in allergy using a dual-reporter system to track IgE plasma cells (PCs) in mice. Short-term allergen exposure resulted in the generation of IgE plasma cells that resided mainly in secondarylymphoid organs and produced IgE that was unable to degranulate mast cells. In contrast, chronic allergen exposure led to the generation of long-lived IgE plasma cells that were primarily derived from sequential class switching of IgG1, accumulated in the bone marrow (BM) and produced IgE capable of inducing anaphylaxis. Most importantly, IgE plasma cells were found in the BM of human allergic, but not non-allergic donors, and allergen-specific IgE produced by these cells was able to induce mast cell degranulation when transferred to mice. These data demonstrate that longlived IgE BMPCs arise during chronic allergen exposure and establish serological memory in both mice and humans.

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