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The Journal of Immunology, 2003, 170: 4630-4637.
Copyright © 2003 by The American Association of Immunologists

IKK{beta} Is Required for Peripheral B Cell Survival and Proliferation1

Zhi-Wei Li*,{dagger}, Sidne A. Omori{dagger},{ddagger}, Tord Labuda2,*,{dagger}, Michael Karin3,*,{dagger} and Robert C. Rickert3,{dagger},{ddagger}

* Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, {dagger} Cancer Center, and {ddagger} Division of Biology, University of California-San Diego, La Jolla, CA 92093

NF-{kappa}B activity in mammalian cells is regulated through the I{kappa}B kinase (IKK) complex, consisting of two catalytic subunits (IKK{alpha} and IKK{beta}) and a regulatory subunit (IKK{gamma}). Targeted deletion of Ikk{beta} results in early embryonic lethality, thus complicating the examination of IKK{beta} function in adult tissues. Here we describe the role of IKK{beta} in B lymphocytes made possible by generation of a mouse strain that expresses a conditional Ikk{beta} allele. We find that the loss of IKK{beta} results in a dramatic reduction in all peripheral B cell subsets due to associated defects in cell survival. IKK{beta}-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-{kappa}B signaling pathway. These findings are consistent with a failure to mount effective Ab responses to T cell-dependent and independent Ags. Thus, IKK{beta} provides a requisite role in B cell activation and maintenance and thus is a key determinant of humoral immunity.




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