First Author | Fukuda T | Year | 1997 |
Journal | J Exp Med | Volume | 186 |
Issue | 3 | Pages | 439-48 |
PubMed ID | 9236196 | Mgi Jnum | J:42667 |
Mgi Id | MGI:1096098 | Doi | 10.1084/jem.186.3.439 |
Citation | Fukuda T, et al. (1997) Disruption of the Bcl6 gene results in an impaired germinal center formation. J Exp Med 186(3):439-48 |
abstractText | The Bcl6 gene has been identified from the chromosomal translocation breakpoint in B cell lymphomas, and its products are expressed highly in germinal center (GC) B cells. To investigate the function of Bcl6 in lymphocytes, we have generated RAG1-deficient mice reconstituted with bone marrow cells from Bcl6-deficient mice (Bcl6(-/-)RM). Lymphogenesis in primary lymphoid tissues of Bcl6(-/-)RM is normal, and Bcl6(-/-)RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens. However, GCs were not found in these mice. This defect was mainly due to the abnormalities of B cells. Therefore, Bcl6 is essential for the differentiation of GC B cells. |