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First published online December 1, 2003
doi: 10.1242/10.1242/jcs.00904

Journal of Cell Science 117, 31-39 (2004)
Published by The Company of Biologists 2004
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Commentary

NF-{kappa}B signaling in lymphocytes: a new cast of characters

Peter C. Lucas1, Linda M. McAllister-Lucas2 and Gabriel Nuñez1,*

1 Department of Pathology, University of Michigan Medical School, 4131 CCGC, 1500 East Medical Center Dr., Ann Arbor, MI 48109, USA
2 Department of Pediatrics, University of Michigan Medical School, 4131 CCGC, 1500 East Medical Center Dr., Ann Arbor, MI 48109, USA

* Author for correspondence (e-mail: bclx{at}umich.edu)

Cell-surface antigen receptors on B and T lymphocytes are complex, multisubunit assemblies that must recruit several accessory proteins and activate multiple signaling pathways in order to illicit a proper immune response. One pathway culminates in the activation of specific protein kinase C (PKC) isoforms, which is necessary for the ultimate activation of the NF-{kappa}B transcription factor. Since NF-{kappa}B plays a crucial role in the adaptive immune response (e.g. in lymphocyte proliferation and cytokine production), it is important to understand the molecular mechanisms by which NF-{kappa}B is regulated. Nevertheless, the connection between PKC activation and NF-{kappa}B has remained a mystery that has now been at least partly solved. Recent findings implicate a new scaffolding protein, Bimp3/CARMA1/CARD11, as a key factor in bridging PKC activation with the downstream activation of Bcl10 and MALT1, which ultimately stimulates NF-{kappa}B. Since some of these signaling components are lymphocyte specific, therapeutic agents that block this pathway could blunt the inappropriate proliferation of lymphocytes associated with certain inflammatory and neoplastic disorders. Alternatively, agents that specifically augment this pathway, thereby enhancing immune function in immunodeficiency, may be developed.

Key words: NF-{kappa}B, PKC{Theta}, Bcl10, MAGUK




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