| First Author | Sun L | Year | 2021 |
| Journal | Cell Rep | Volume | 35 |
| Issue | 9 | Pages | 109188 |
| PubMed ID | 34077723 | Mgi Jnum | J:314768 |
| Mgi Id | MGI:6717087 | Doi | 10.1016/j.celrep.2021.109188 |
| Citation | Sun L, et al. (2021) Transcription factor Ascl2 promotes germinal center B cell responses by directly regulating AID transcription. Cell Rep 35(9):109188 |
| abstractText | During germinal center (GC) reactions, activated B cells undergo clonal expansion and functional maturation to produce high-affinity antibodies and differentiate into plasma and memory cells, accompanied with class-switching recombination (CSR) and somatic hypermutation (SHM). Activation-induced cytidine deaminase (AID) is responsible for both CSR and SHM in GC B cells. Transcriptional mechanisms underlying AID regulation and GC B cell reactions are still not well understood. Here, we show that expression of Ascl2 transcription factor is upregulated in GC B cells. Ectopic expression of Ascl2 promotes GC B cell development and enhances antibody production and affinity maturation. Conversely, deletion of Ascl2 in B cells impairs the GC response. Genome-wide analysis reveals that Ascl2 directly regulates GC B cell-related genes, including AID; ectopic expression of AID in Ascl2-deficient B cells rescues their antibody defects. Thus, Ascl2 regulates AID transcription and promotes GC B cell responses. |
