| First Author | Li ZW | Year | 2003 |
| Journal | J Immunol | Volume | 170 |
| Issue | 9 | Pages | 4630-7 |
| PubMed ID | 12707341 | Mgi Jnum | J:82995 |
| Mgi Id | MGI:2656420 | Doi | 10.4049/jimmunol.170.9.4630 |
| Citation | Li ZW, et al. (2003) IKK beta is required for peripheral B cell survival and proliferation. J Immunol 170(9):4630-7 |
| abstractText | NF-kappaB activity in mammalian cells is regulated through the IkappaB kinase (IKK) complex, consisting of two catalytic subunits (IKKalpha and IKKbeta) and a regulatory subunit (IKKgamma). Targeted deletion of Ikkbeta results in early embryonic lethality, thus complicating the examination of IKKbeta function in adult tissues. Here we describe the role of IKKbeta in B lymphocytes made possible by generation of a mouse strain that expresses a conditional Ikkbeta allele. We find that the loss of IKKbeta results in a dramatic reduction in all peripheral B cell subsets due to associated defects in cell survival. IKKbeta-deficient B cells are also impaired in mitogenic responses to LPS, anti-CD40, and anti-IgM, indicating a general defect in the ability to activate the canonical NF-kappaB signaling pathway. These findings are consistent with a failure to mount effective Ab responses to T cell-dependent and independent Ags. Thus, IKKbeta provides a requisite role in B cell activation and maintenance and thus is a key determinant of humoral immunity. |
