| Literature DB >> 26116508 |
Hans D Brightbill1, Janet K Jackman2, Eric Suto3, Heather Kennedy4, Charles Jones4, Sreedevi Chalasani4, Zhonghua Lin3, Lucinda Tam5, Meron Roose-Girma5, Mercedesz Balazs3, Cary D Austin4, Wyne P Lee3, Lawren C Wu1.
Abstract
NF-κB-inducing kinase (NIK) is a primary regulator of the noncanonical NF-κB 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-κB pathway in mice.Entities:
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Year: 2015 PMID: 26116508 DOI: 10.4049/jimmunol.1401514
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422