<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/DRR066/DRR066829/DRR066829.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR066/DRR066831/DRR066831.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/DRR066/DRR066830/DRR066830.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>Kazusa DNA Research Institute</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJDB5073</full_dataset_link><scientific_name>Mus musculus</scientific_name><long_description>Virus infection induces T follicular helper (TFH) and T helper 1 (TH1) cells. Although TFH cells are important in anti-viral humoral immunity, the role of TH 1 cells is still elusive. IgG2 antibodies predominate in the response to vaccination with inactivated Influenza A virus (IAV) and were responsible for protective immunity to lethal challenge with pathogenic H5N1 and pandemic H1N1 IAVs even in mice lacking TFH cells owing to B or T cell-specific ablation of the Bcl6. B cells of wild type (WT) and conditional Bcl6-/- mice were sorted and the transcription of IgG were analyzed by using Illumina MiSeq.</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Mus musculus</name><description>Next Generation Sequencing Facilitates Quantitative Analysis of IgG transcription in Wild Type and Bcl6-/- B cells</description><dates><last_updated>2025-09-24</last_updated><first_public>2016-10-15</first_public></dates><accession>PRJDB5073</accession><cross_references><taxon>10090</taxon></cross_references></HashMap>