<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/055/SRR32589055/SRR32589055_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/052/SRR32589052/SRR32589052_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/053/SRR32589053/SRR32589053_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/054/SRR32589054/SRR32589054_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/055/SRR32589055/SRR32589055_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/053/SRR32589053/SRR32589053_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/052/SRR32589052/SRR32589052_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR325/054/SRR32589054/SRR32589054_1.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Pediatrics, University of Pittsburgh</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA1232619</full_dataset_link><scientific_name>Mus musculus</scientific_name><tag>xref:PubMed:40297693</tag><long_description>Type 2 inflammation in the lung underlies allergic asthma and promotes tumor metastasis. Type 2 innate lymphoid cells (ILC2s) respond to tissue damage signals including IL-33 and IL-25 and are implicated in type 2 inflammatory diseases of the lung, but the factors that maintain ILC2s ability to produce type 2 cytokines are not known. We show Blimp-1 is a key transcriptional repressor of type 1 genes induced by the type 2 cytokine IL-9 in ILC2s in response to tissue damage signals. Loss of Blimp-1 in ILC2s altered inflammation in response to allergens, but also limited metastatic melanoma in the lung by limiting type 2 cytokines in favor of type I cytokines including IFNg and TNF. Thus, Blimp-1 protects the type 2 identity of ILC2s during lung inflammatory diseases. Overall design: 2 female Blimp-1IL7RaCre and 2 female ControlIL7RaCre mice match with age were used. Whole lung was harvested and ILC2s were sorted from lung by the following markers: live, lineage-, CD90.2+, CD3-. After sorting, ~15,000 ILC2s cells from each sample were cultured in complete RPMI in 96-well plate with 20ng/mL IL-33 and 20ng/mL IL-25 for 72 hours. After 72 hours, ILC2s were collected passed down for sequencing.</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Blimp-1 protects the transcriptional identity of group 2 innate lymphocytes in lung inflammation [ATAC-seq]</name><description>Blimp-1 protects the transcriptional identity of group 2 innate lymphocytes in lung inflammation [ATAC-seq]</description><dates><last_updated>2025-09-24</last_updated><first_public>2025-05-09</first_public></dates><accession>PRJNA1232619</accession><cross_references><GEO>GSE291230</GEO><taxon>10090</taxon><PubMed>40297693</PubMed></cross_references></HashMap>