Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA237583 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The mechanisms that guide Th2 cell differentiation in barrier tissues are unclear but important for the development of allergic asthma. Using temporal, spatial and single cell transcriptomic tracking of house dust mite (HDM) specific T cells, we describe the molecular pathways driving allergen-specific Th2 cells. Early Blimp-1 expression occurs in a subset of CD4 T cells in the lymph node prior to lung migration driven by IL-10 from allergen-specific T cells, but was not required for GATA3 upregulation. Instead, IL-2 via STAT5 was required to directly repress Bcl6 and Bach2 to support GATA3 and Blimp-1 upregulation. Loss of Blimp-1 during priming in the lymph node ablated the formation of Th2 cells that migrate to the lung, indicating early Blimp-1 promotes the population of Th2 cells with migratory capability. Spatial microniches of IL-2 in the lymph node discriminate and support these earliest Blimp-1+ migratory Th2 cells, demonstrating that lymph node localization is a primary driver of differentiation. Our findings illuminate the molecular pathways for inhaled allergens to promote Th2 cells and identify an early requirement for IL-2 mediated spatial microniches and allergen-driven IL-10 from responding T cells that drive allergic asthma.
2024-02-20 | GSE245111 | GEO
Project description:The mechanisms that guide Th2 cell differentiation in barrier tissues are unclear but important for the development of allergic asthma. Using temporal, spatial and single cell transcriptomic tracking of house dust mite (HDM) specific T cells, we describe the molecular pathways driving allergen-specific Th2 cells. Early Blimp-1 expression occurs in a subset of CD4 T cells in the lymph node prior to lung migration driven by IL-10 from allergen-specific T cells, but was not required for GATA3 upregulation. Instead, IL-2 via STAT5 was required to directly repress Bcl6 and Bach2 to support GATA3 and Blimp-1 upregulation. Loss of Blimp-1 during priming in the lymph node ablated the formation of Th2 cells that migrate to the lung, indicating early Blimp-1 promotes the population of Th2 cells with migratory capability. Spatial microniches of IL-2 in the lymph node discriminate and support these earliest Blimp-1+ migratory Th2 cells, demonstrating that lymph node localization is a primary driver of differentiation. Our findings illuminate the molecular pathways for inhaled allergens to promote Th2 cells and identify an early requirement for IL-2 mediated spatial microniches and allergen-driven IL-10 from responding T cells that drive allergic asthma.
2024-02-20 | GSE245110 | GEO
Project description:The mechanisms that guide Th2 cell differentiation in barrier tissues are unclear but important for the development of allergic asthma. Using temporal, spatial and single cell transcriptomic tracking of house dust mite (HDM) specific T cells, we describe the molecular pathways driving allergen-specific Th2 cells. Early Blimp-1 expression occurs in a subset of CD4 T cells in the lymph node prior to lung migration driven by IL-10 from allergen-specific T cells, but was not required for GATA3 upregulation. Instead, IL-2 via STAT5 was required to directly repress Bcl6 and Bach2 to support GATA3 and Blimp-1 upregulation. Loss of Blimp-1 during priming in the lymph node ablated the formation of Th2 cells that migrate to the lung, indicating early Blimp-1 promotes the population of Th2 cells with migratory capability. Spatial microniches of IL-2 in the lymph node discriminate and support these earliest Blimp-1+ migratory Th2 cells, demonstrating that lymph node localization is a primary driver of differentiation. Our findings illuminate the molecular pathways for inhaled allergens to promote Th2 cells and identify an early requirement for IL-2 mediated spatial microniches and allergen-driven IL-10 from responding T cells that drive allergic asthma.
2024-02-26 | GSE245109 | GEO
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:Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response. Comparison of methylation profiles from allergens 2,4-dinitrochlorobenzene (DNCB; a contact allergen) and trimellitic anhydride (TMA; a respiratory allergen) or vehicle acetone:olive oil (AOO).
2014-02-07 | E-GEOD-54768 | biostudies-arrayexpress
Project description:Alterations of DNA methylome during chemical carcinogenesis
| PRJNA176928 | ENA
Project description:T helper type 2 (Th2) responses are induced by protease allergens and helminthes. However the molecular mechanisms that initiate Th2 responses are poorly understood. To obtain insight into this mechanism, we performed a microarray analysis of lymph node DCs stimulated in vitro with the protease allergen papain, or with LPS, a Th1 inducing stimulus. Key words: Th2 response, LPS, dendritic cells, Papain
2010-05-05 | GSE21602 | GEO
Project description:Culture-expanded mouse lymph node-derived fibroblastic reticular cells
| PRJNA257501 | ENA
Project description:Identification of chemical allergen inducible genes in mouse skin. Ear samples were isolated from CL57BL/6 mice 6 hours after topical application of a prototypic chemical allergen, a skin irritant or vehicle alone. Total RNA were extracted from ear skin samples treated with a chemical allergen, a skin irritant, or vehicle alone for 6 hours.
2011-03-10 | E-GEOD-20726 | biostudies-arrayexpress
Project description:Gene expression analysis of mouse ear samples treated with chemical allergen
| PRJNA124953 | ENA