| First Author | Brightbill HD | Year | 2015 |
| Journal | J Immunol | Volume | 195 |
| Issue | 3 | Pages | 953-64 |
| PubMed ID | 26116508 | Mgi Jnum | J:240453 |
| Mgi Id | MGI:5883527 | Doi | 10.4049/jimmunol.1401514 |
| Citation | Brightbill HD, et al. (2015) Conditional Deletion of NF-kappaB-Inducing Kinase (NIK) in Adult Mice Disrupts Mature B Cell Survival and Activation. J Immunol 195(3):953-64 |
| abstractText | NF-kappaB-inducing kinase (NIK) is a primary regulator of the noncanonical NF-kappaB signaling pathway, which plays a vital role downstream of BAFF, CD40L, lymphotoxin, and other inflammatory mediators. Germline deletion or inactivation of NIK in mice results in the defective development of B cells and secondary lymphoid organs, but the role of NIK in adult animals has not been studied. To address this, we generated mice containing a conditional allele of NIK. Deletion of NIK in adult mice results in decreases in B cell populations in lymph nodes and spleen, similar to what is observed upon blockade of BAFF. Consistent with this, B cells from mice in which NIK is acutely deleted fail to respond to BAFF stimulation in vitro and in vivo. In addition, mice with induced NIK deletion exhibit a significant decrease in germinal center B cells and serum IgA, which is indicative of roles for NIK in additional pathways beyond BAFF signaling. Our conditional NIK-knockout mice may be broadly useful for assessing the postdevelopmental and cell-specific roles of NIK and the noncanonical NF-kappaB pathway in mice. |
