Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE288454 | GEO | 2025/03/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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 of lung-resident memory B cells early after allergen inhalation (day21) and late (day 77) to explore potential mechanisms that control residency in the lungs.

2025-03-25 | GSE288495 | GEO

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.

| PRJNA1217786 | ENA

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.

| PRJNA1217864 | ENA

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.

2023-05-15 | GSE231427 | GEO

CD23+IgG1+ memory B cells are poised to switch to pathogenic IgE production in food allergy

Project description:Food allergy is caused by allergen-specific IgE but little is known about the B cell memory of persistent responses. Here we describe in pediatric peanut allergy a population of CD23+IgG1 memory B cells that contains peanut-specific clones and generates IgE plasma cells on activation. Through single cell transcriptomics and B cell receptor (BCR) sequencing, we characterized FCER2/CD23+ IgG1 memory B cells co-expressing IL4R, IL13RA1, IGHE and carrying highly mutated BCRs. Further we found that peanut allergen (Ara h 2)-specific B cells were mostly IgG1 memory cells, carried highly mutated BCRs compared to diphtheria toxin-specific B cells, and expressed FCER2 and germlin IGHE. Our findings suggest that CD23+IgG1+ memory B cells transcribing IGHE are a unique memory population containing precursors for pathogenic IgE in food allergy.

2023-11-16 | GSE208235 | GEO

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

Project description:Allergen-specific IgE antibodies mediate allergic pathology in diseases such as allergic rhinitis and food allergy. Memory B cells (MBCs) contribute to circulating IgE by regenerating IgE-producing plasma cells upon allergen encounter. We report a population of type 2 polarized MBCs defined as CD23hi, IL-4Rαhi, CD32low at the transcriptional and surface protein levels.

2023-11-25 | GSE248256 | GEO

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.

2019-11-16 | GSE140435 | GEO

Identification of a T follicular helper subset that drives anaphylactic IgE

Project description:We report a rare population of IL-13-producing Tfh cells that were present with high-affinity IgE to allergens. These “Tfh13” cells have an unusual cytokine profile (IL-13hiIL-4hiIL-5hiIL-21lo), co-express BCL6 and GATA3 and were required for production of high- but not low-affinity IgE and accordingly, allergen-induced anaphylaxis.

2019-08-06 | GSE132798 | GEO

Induction of natural IgE by glucocorticoids

Project description:Allergy is one of the most prevalent chronic diseases, affecting hundreds of millions of people worldwide. In allergy, environmental allergens induce B cells to undergo class switch recombination and produce Immunoglobulin E (IgE) antibodies. IgE is a key molecule that mediates allergic responses by coating mast cell or basophil surfaces and inducing degranulation upon binding a specific allergen. IgE can also be spontaneously produced in the absence of exogenous allergens, yet the origin, regulation, and functions of such “natural” IgE still remains largely unknown. Here, we discovered that glucocorticoids, which are steroid stress hormones, enhance IgE isotype class switching in B cells both in vivo and ex vivo without antigenic challenge. Such IgE class switching is promoted by B cell-intrinsic glucocorticoid receptor signaling that reinforces CD40 signaling and synergizes with the IL-4/STAT6 pathway. In addition, we found that rare B cells in the mesenteric lymph nodes are responsible for the production of glucocorticoid-inducible IgE. Furthermore, we showed that locally produced glucocorticoids in the gut may induce natural IgE during perturbations of gut homeostasis such as dysbiosis. Notably, mice preemptively treated with glucocorticoids were protected from subsequent IgE-mediated pathogenic anaphylaxis in vivo. Together, our results suggest that glucocorticoids, classically considered to be broadly immunosuppressive, have a selective immunostimulatory role in B cells.

2022-09-09 | GSE203542 | 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.

2024-01-22 | GSE221310 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data