{"database":"GEO","file_versions":[],"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=GSE316969"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"IL-9 and Blimp-1 protects the transcriptional identity of group 2 innate lymphocytes in allergic asthma","description":"Allergic asthma is driven by type 2 immune responses, including those mediated by type 2 innate lymphoid cells (ILC2s). Although ILC2s are activated by the tissue alarmins IL-33 and IL-25, these signals do not intrinsically enforce type 2 identity, and the mechanisms that maintain type 2 cytokine expression remain unclear. Here we show that allergen-induced IL-33 and IL-25 rapidly induce IL-9, which in turn upregulates the transcriptional repressor Blimp-1 in ILC2s. Blimp-1 sustains type 2 immunity by directly repressing type 1 inflammatory programs, including expression of IFNg and TNF. Deletion of Blimp-1 in ILC2s increased type 1 cytokine production and reduced IL-5 and IL-13 expression, eosinophil recruitment, and mucus production in the lung. In contrast, IL-9 expression was enhanced in the absence of Blimp-1, leading to increased mast cell recruitment. Together, these findings identify Blimp-1 as a key regulator of ILC2 transcriptional fidelity that stabilizes type 2 inflammation while constraining divergent inflammatory programs during allergic responses.","dates":{"publication":"2026/04/16"},"accession":"GSE316969","cross_references":{"GSM":["GSM9463226","GSM9463227","GSM9463228"],"GPL":["34290"],"GSE":["316969"],"taxon":["Mus musculus"]}}