{"database":"GEO","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"species":["Mus musculus"," blank sample"],"gds_type":["Protein profiling by protein array"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE296597"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Essential Role of Apoptosis in Immature B Cells for Preventing Autoimmune Disease in Mice","description":"Autoreactive B cells are generated through V(D)J recombination during development and somatic hypermutation during immune responses. Clonal deletion via programmed cell death is a key mechanism to eliminate these cells, as evidenced by autoimmune disease development in mice with defective B cell apoptosis. However, the specific stages of B cell development or activation where autoreactive B cells are deleted to prevent autoimmune diseases remain unclear. Here, we directed anti-apoptotic Bcl-2 expression to early B cell progenitors in the bone marrow and to activated B cells.Our findings revealed that Bcl-2 expression during B cell development expanded peripheral transitional, anergic and follicular, but not bone marrow immature B cells. Follicular and anergic B cell accumulation were partly due to increased production.Notably, Bcl-2 expression during development, but not during activation, caused an antibody-dependent autoimmune disease with a specific autoantibody profile. Thus, peripheral transitional B cells are particularly sensitive to apoptosis and disrupting immature B cell apoptosis allows autoreactive clones derived from V(D)J recombination to enter mature and activated B cell repertoires to promote autoimmune disease.","dates":{"publication":"2026/05/11"},"accession":"GSE296597","cross_references":{"GSM":["GSM8973249","GSM8973248","GSM8973250","GSM8973252","GSM8973251","GSM8973254","GSM8973253","GSM8973245","GSM8973256","GSM8973255","GSM8973247","GSM8973246"],"GPL":["29507"],"GSE":["296597"],"taxon":["Mus musculus"," blank sample"]}}