GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339436/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339436GEOGSEfalseCD97/ADGRE5 attenuates the induction of adaptive type 2 immune responses in allergic asthmaAllergic 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.2026/08/03GSE339436GSM9895781GSM9895780GSM9895779GSM9895778GSM9895777GSM9895776GSM9895775GSM989577424247339436Mus musculus