| First Author | Ren H | Year | 2002 |
| Journal | J Immunol | Volume | 168 |
| Issue | 2 | Pages | 577-87 |
| PubMed ID | 11777949 | Mgi Jnum | J:131003 |
| Mgi Id | MGI:3772643 | Doi | 10.4049/jimmunol.168.2.577 |
| Citation | Ren H, et al. (2002) I-kappa B kinase beta is critical for B cell proliferation and antibody response. J Immunol 168(2):577-87 |
| abstractText | The NF-kappaB proteins are critical in the regulation of the immune and inflammatory response. Stimulation of the NF-kappaB pathway leads to increases in I-kappaB kinase beta (IKKbeta) kinase activity to result in the enhanced phosphorylation and degradation of I-kappaB and the translocation of the NF-kappaB proteins from the cytoplasm to the nucleus. In this study, a dominant-negative IKKbeta mutant expressed from the IgH promoter was used to generate transgenic mice to address the role of IKKbeta on B cell function. Although these transgenic mice were defective in activating the NF-kappaB pathway in B cells, they exhibited no defects in B lymphocyte development or basal Ig levels. However, they exhibited defects in the cell cycle progression and proliferation of B cells in response to treatment with LPS, anti-CD40, and anti-IgM. Furthermore, selective defects in the production of specific Ig subclasses in response to both T-dependent and T-independent Ags were noted. These results suggest that IKKbeta is critical for the proliferation of B cells and the control of some aspects of the humoral response. |
