GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE296nnn/GSE296597/primaryOK200ProteomicsMus musculus blank sampleProtein profiling by protein arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE296597GEOGSEfalseEssential Role of Apoptosis in Immature B Cells for Preventing Autoimmune Disease in MiceAutoreactive 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.2026/05/11GSE296597GSM8973249GSM8973248GSM8973250GSM8973252GSM8973251GSM8973254GSM8973253GSM8973245GSM8973256GSM8973255GSM8973247GSM897324629507296597Mus musculus blank sample