Single cell RNAseq of murine dendritic cells in presence or absence of Il13ra1
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE227209 | GEO | 2026/07/01
REPOSITORIES: GEO
Similar Datasets
Project description:We used RNA sequencing to study gene expression in lymph node derived DCs from anaphylactic mice sensitized intranasally with the major peach allergen Pru p 3, during the acute reaction phase, induced intraperitoneally. In total, 237 genes changed significantly, 181 showing at least two-fold changes. Almost three quarters of these increased during anaphylaxis
2018-11-30 | GSE123127 | GEO
Project description:Skin barrier dysfunction in the setting of atopic dermatitis (AD) leads to cutaneous allergen sensitization (CAS).1 The atopic march hypothesis proposes that CAS leads to the subsequent development of other allergic disorders such as asthma and food allergy.2-5 The latter is associated with IgE-mediated anaphylaxis6. However, the precise mechanisms by which CAS promotes IgE-mediated allergic responses remain unclear. We thus established a CAS model of anaphylaxis and identified a unique role of the Interleukin (IL)-13 signal in DCs to generate anaphylactic IgE responses. Single-cell RNA-seq revealed the emergence of IL-13 receptor alpha 1 chain (IL-13Rα1)-expressing type 2 conventional dendritic cells (cDC2s) in CAS. Similar DC populations were identified in allergic rhinitis humans with cedar pollan-specific IgE antibodies. Lineage-specific disruption of IL-13 signaling resulted in a marked reduction in cDC2s that highly expressed MHC class II: these cells controlled the germinal center entry of TFH cells required for IgE responses. These data reveal a unique role for IL-13 in controlling the expansion of MHCIIhi cDC2s and associated TFH cell responses in the setting of allergy.
2026-07-01 | GSE274017 | GEO
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 â 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive.
2010-06-24 | E-GEOD-13380 | biostudies-arrayexpress
Project description:Expression of Blimp-1 was specifically deleted in dendritic cells (DCs) by breeding Blimp-1 flox and CD11c-CRE mice. MiRNA expression was evaluated and compared from DCs, CD4+ T cells and total B cells from spleens of control and Blimp-1 KO mice.
2013-09-05 | GSE40587 | GEO
Project description:Shellfish allergy is a significant public health concern, yet the molecular basis of allergenicity in molluscs remains poorly defined. In this study, we performed an in-depth proteomic and immunoinformatic analysis of two widely consumed blood clam species, Anadara broughtonii and Tegillarca granosa, to identify and characterize novel allergen candidates. Using high-resolution tandem mass spectrometry, we generated comprehensive protein profiles and applied three complementary allergen prediction algorithms (SEP-AlgPro™, AllerCatPro,and AlgPred 2.0) to screen for potential IgE-binding proteins. Immunoblotting with sera from shrimp-sensitized individuals confirmed IgE reactivity for nine proteins, including catalase and several hemoglobin isoforms—none of which are currently recognized as molluscan allergens. Homology modeling and sequence alignment revealed conserved structural motifsimplicated in allergenicity and suggested cross-reactivity with known crustacean allergens. These findings expand the repertoire of putative molluscan allergens and demonstrate theutility of integrated proteomic and immunoinformatic strategies for allergen discovery.
2025-08-11 | PXD064892 | Pride
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 – 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma
2008-11-04 | GSE13380 | GEO
Project description:To study the plasticity of IgE-fated allergen-specific responses, we employed various immunization methods to model type 1 and type 2 immune responses in mice, along with antibody (Ab)-mediated blockade of signaling receptors. Here, we treated epicutaneously sensitized mice with anti-IL-4Ra or an isotype control prior to s.c. reexposures and then performed paired single-cell RNA- and BCR-sequencing on B cells. An additional group of mice were administered cholera toxin and OVA to model a classical type 2 immunization strategy.
2025-11-13 | E-MTAB-15982 | biostudies-arrayexpress
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
Project description:Dendritic cells (DCs) in tissues and lymphoid organs comprise distinct functional subsets that differentiate in situ from circulating progenitors. Tissue-specific signals that regulate DC subset differentiation are poorly understood. We report that DC-specific deletion of the Notch2 receptor caused a reduction of DC populations in the spleen. Within the splenic CD11b+ DCs, Notch signaling blockade ablated a distinct population marked by high expression of adhesion molecule Esam. The Notch-dependent Esamhi DC subset also required lymphotoxin beta receptor signaling, proliferated in situ and facilitated efficient CD4+ T cell priming. The Notch-independent Esamlo DCs expressed monocyte-related genes and showed superior cytokine responses. In addition, Notch2 deletion led to the loss of CD11b+ CD103+ DCs in the intestinal lamina propria and to the corresponding decrease of IL-17-producing CD4+ T cells in the intestine. Thus,Notch2 is a common differentiation signal for T cell-priming CD11b+ DC subsets in the spleen and intestine. We compared genome-wide expression profiles of wild-type Esam(hi) and Esam(lo) splenic CD11b+ DC populations, along with CD11b+ DCs from DC-RBPJΔ mice. Spleens from 2-3 Cx3cr1-GFP+ RBPJflox/flox CD11c-Cre+ mice or Cx3cr1-GFP+ RBPJflox/flox Cre-negative littermate controls were isolated, pooled and depleted of lymphoid and erythroid cells by negative selection on MACS columns. Live cells were stained for surface expression of CD11c, CD11b and Esam. CD11c(hi) CD11b+ DCs from control mice could be separated into Esam(lo) GFP(hi) versus Esam(hi) GFP(lo) subsets. CD11c(hi) CD11b+ DCs from RBPJ-targeted mice spleens were uniformly Esam(lo) GFP(hi). The two subsets from control mice and single Esam(lo) GFP(hi) subset from RBPJ-targeted mice were sorted using FACSAria II flow sorter and analyzed using GeneChip Mouse Gene 1.0 ST Array (Affymetrix).
2011-10-31 | E-GEOD-31551 | biostudies-arrayexpress