<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/GSE312nnn/GSE312785/</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=GSE312785</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA-seq analysis of splenic IgG1 or IgM plasma cells</name><description>In a typical primary immune response, the BCR is brought about by IgM to IgG isotype switching, wherein B cells switched to IgG give rise to more long-lived plasma cells (LLPCs). How such isotype-driven bias takes place still remains unclear. Here, we showed that IgG1 germinal center (GC) B cells presented higher levels of antigens to Tfh cells, making the resultant plasma cells more proliferate than IgM ones, and that BCR signal through IgM conferred more Bim-dependent apoptosis on their plasma cells, together dominating the numbers of IgG1 over IgM plasma cells in the secondary lymphoid tissues. In addition, IgG1 plasma cells were more prone to migrate to bone marrow than IgM ones. Hence, our findings suggest that differential activities in antigen presentation and signaling through IgG1 type BCRs contribute to enrichment of IgG1 plasma cells in the bone marrow long-lived plasma cell compartment.</description><dates><publication>2026/07/11</publication></dates><accession>GSE312785</accession><cross_references><GSM>GSM9353207</GSM><GSM>GSM9353205</GSM><GSM>GSM9353206</GSM><GSM>GSM9353203</GSM><GSM>GSM9353204</GSM><GSM>GSM9353202</GSM><GPL>24247</GPL><GSE>312785</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>