{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339436/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339436"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"CD97/ADGRE5 attenuates the induction of adaptive type 2 immune responses in allergic asthma","description":"Allergic asthma results from an uncontrolled type 2 immune response to inhaled allergens. Here, we investigate the role of CD97/ADGRE5, expressed in mouse and human immune and lung epithelial cells, in this disease. Female Cd97-/- mice exhibit an exacerbated asthmatic phenotype across multiple models, primarily due to CD97 loss on immune cells. A single CD97 antibody treatment before allergen sensitization worsens allergic responses, highlighting a role for CD97 in early immune regulation. Post-sensitization, Cd97-/- mice display higher frequencies of lung conventional type 2 and monocyte-derived dendritic cells (DCs). Allergen-pulsed Cd97-/- bone marrow-derived DCs are more activated, promote enhanced proliferation and type 2 cytokine secretion by CD4⁺ OT-II cells, and induce stronger airway inflammation. Consistently, ADGRE5 expression is reduced in airway mucosa-derived mononuclear phagocyte subsets in human asthmatics after allergen-induced exacerbation. These results identify CD97 as a key regulator of DC-driven type 2 allergic responses and a potential target in asthma.","dates":{"publication":"2026/08/03"},"accession":"GSE339436","cross_references":{"GSM":["GSM9895781","GSM9895780","GSM9895779","GSM9895778","GSM9895777","GSM9895776","GSM9895775","GSM9895774"],"GPL":["24247"],"GSE":["339436"],"taxon":["Mus musculus"],"PMID":["[42660929]"]}}