期刊
JOURNAL OF IMMUNOLOGY
卷 195, 期 3, 页码 953-964出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401514
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资金
- Genentech Inc.
NF-kappa B-inducing kinase (NIK) is a primary regulator of the noncanonical NF-kappa B 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-kappa B pathway in mice.
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