| First Author | Hahn M | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 3 | Pages | 732-41 |
| PubMed ID | 26593098 | Mgi Jnum | J:234574 |
| Mgi Id | MGI:5790282 | Doi | 10.1002/eji.201546081 |
| Citation | Hahn M, et al. (2016) NF-kappaB-inducing kinase is essential for B-cell maintenance in mice. Eur J Immunol 46(3):732-41 |
| abstractText | NF-kappaB-inducing kinase (NIK) is a key mediator of the noncanonical NF-kappaB signaling pathway, which is critical for normal B-cell development and function. It is well established that the complete deletion of NIK in mice results in defective B cells and impaired secondary lymphoid organogenesis. To address the role of NIK deficiency specifically in B cells, we generated a new mouse strain for the conditional deletion of this kinase. Deletion of NIK during B-cell development results in a drastic reduction of mature B cells from the transitional 2 stage on, while B-1 B cells are less affected. Moreover, deletion of NIK in the germinal centers decreases the numbers of germinal center B cells and impairs the ability of NIK-deficient B cells to develop into class-switched cells in vivo. This new mouse strain will be helpful for studying the role of NIK in different cell types of the body. |
