<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE304nnn/GSE304046/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304046</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>A Neuroimmune Circuit that Regulates Allergic Inflammation in the Esophagus in Mice</name><description>Eosinophilic esophagitis (EoE) is a chronic, allergic disease associated with refractory pain in patients, yet the function of the nervous system in EoE pathogenesis remains ill-defined. Here we elucidate a mouse neuroimmune circuit that is linked to type 2-associated allergic inflammation and clinical responses in the esophagus, including pain. In a mouse allergy model, allergen exposure evokes pain-like behavior, increases esophageal Nav1.8+ sensory innervation density, and alters nociceptor sensitization. Thoracic dorsal root ganglia (DRG) show allergen-induced expression of type 2 cytokine receptors Il4ra and Il13ra1, while IL-4 and IL-13 sensitize DRG neurons to noxious agents. Mechanistically, conditional deletion of Il4ra in mouse NaV1.8+ neurons attenuate the above allergen-induced phenotypes as well as the levels of insulin-like growth factor 1 (IGF1); in parallel, IGF-1 receptor inhibition also dampens these disease features. Finally, EoE patient samples show increased esophageal neuronal density when compared with controls. Our findings thus describe a type 2 neuroimmune circuit that potentially contributes to EoE pathogenesis, including pain.</description><dates><publication>2026/08/25</publication></dates><accession>GSE304046</accession><cross_references><GSM>GSM9141696</GSM><GSM>GSM9141652</GSM><GSM>GSM9141651</GSM><GSM>GSM9141695</GSM><GSM>GSM9141654</GSM><GSM>GSM9141698</GSM><GSM>GSM9141653</GSM><GSM>GSM9141697</GSM><GSM>GSM9141692</GSM><GSM>GSM9141691</GSM><GSM>GSM9141650</GSM><GSM>GSM9141694</GSM><GSM>GSM9141693</GSM><GSM>GSM9141690</GSM><GSM>GSM9141649</GSM><GSM>GSM9141648</GSM><GSM>GSM9141689</GSM><GSM>GSM9141688</GSM><GSM>GSM9141663</GSM><GSM>GSM9141662</GSM><GSM>GSM9141665</GSM><GSM>GSM9141664</GSM><GSM>GSM9141661</GSM><GSM>GSM9141660</GSM><GSM>GSM9141659</GSM><GSM>GSM9141656</GSM><GSM>GSM9141699</GSM><GSM>GSM9141655</GSM><GSM>GSM9141658</GSM><GSM>GSM9141657</GSM><GSM>GSM9141674</GSM><GSM>GSM9141673</GSM><GSM>GSM9141676</GSM><GSM>GSM9141675</GSM><GSM>GSM9141670</GSM><GSM>GSM9141672</GSM><GSM>GSM9141671</GSM><GSM>GSM9141708</GSM><GSM>GSM9141707</GSM><GSM>GSM9141709</GSM><GSM>GSM9141704</GSM><GSM>GSM9141703</GSM><GSM>GSM9141706</GSM><GSM>GSM9141705</GSM><GSM>GSM9141667</GSM><GSM>GSM9141700</GSM><GSM>GSM9141666</GSM><GSM>GSM9141702</GSM><GSM>GSM9141669</GSM><GSM>GSM9141668</GSM><GSM>GSM9141701</GSM><GSM>GSM9141685</GSM><GSM>GSM9141684</GSM><GSM>GSM9141687</GSM><GSM>GSM9141686</GSM><GSM>GSM9141681</GSM><GSM>GSM9141680</GSM><GSM>GSM9141683</GSM><GSM>GSM9141682</GSM><GSM>GSM9141715</GSM><GSM>GSM9141714</GSM><GSM>GSM9141717</GSM><GSM>GSM9141716</GSM><GSM>GSM9141711</GSM><GSM>GSM9141678</GSM><GSM>GSM9141710</GSM><GSM>GSM9141677</GSM><GSM>GSM9141713</GSM><GSM>GSM9141679</GSM><GSM>GSM9141712</GSM><GPL>34328</GPL><GSE>304046</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>