Stevens S, Ong J, Kim U, Eckhardt L A, Roeder R G
Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10021, USA.
J Immunol. 2000 May 15;164(10):5306-12. doi: 10.4049/jimmunol.164.10.5306.
OCA-B (alternately called Bob1 and OBF-1) is a B cell-specific coactivator that interacts with the ubiquitously expressed Oct-1 and the B cell-restricted Oct-2 to activate transcription via the octamer site (5'-ATGCAAAT-3'). OCA-B-/- mice appear to undergo normal Ag-independent B cell maturation. However, Ag-dependent B cell differentiation, including germinal center formation, production of secondary Ig isotypes, and proliferation in response to surface Ig cross-linking, is greatly affected. We demonstrate that the observed reductions in expression of class-switched isotypes in OCA-B-/- mice may be due in part to deficiencies in the function of the 3'-IgH enhancer elements. Furthermore, we find that surface Ig cross-linking represses all the Ig enhancers and that this repression is absent in OCA-B-/- B cells. These results suggest an important role for OCA-B in Ig enhancer function in vivo.
OCA-B(也称为Bob1和OBF-1)是一种B细胞特异性共激活因子,它与广泛表达的Oct-1以及B细胞限制性的Oct-2相互作用,通过八聚体位点(5'-ATGCAAAT-3')激活转录。OCA-B基因敲除小鼠似乎经历正常的非抗原依赖性B细胞成熟过程。然而,抗原依赖性B细胞分化,包括生发中心形成、次级Ig同种型的产生以及对表面Ig交联的增殖反应,受到极大影响。我们证明,在OCA-B基因敲除小鼠中观察到的类别转换同种型表达降低可能部分归因于3'-IgH增强子元件功能的缺陷。此外,我们发现表面Ig交联会抑制所有Ig增强子,而这种抑制在OCA-B基因敲除的B细胞中不存在。这些结果表明OCA-B在体内Ig增强子功能中起重要作用。