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Trends Immunol. 2008 Jul;29(7):329-36. doi: 10.1016/j.it.2008.03.005. Epub 2008 Jun 3.

Turning NF-kappaB and IRFs on and off in DC.

Author information

1
Laboratory for Host Defense, RIKEN Research Center for Allergy and Immunology, Yokohama city, Kanagawa 230-0045, Japan. tkaisho@rcai.riken.jp

Abstract

Dendritic cells (DCs) produce an array of cytokines after detecting various immune adjuvants through pattern recognition receptors (PRRs). PRR signaling leads to activation of transcription factors such as NF-kappaB or interferon regulatory factors (IRFs) but after activation must be attenuated to avoid immunopathology and to maintain tissue homeostasis. IkappaB kinase family members, originally identified as classical NF-kappaB activators, are now found to be broadly and crucially involved in PRR signaling in a member-specific manner. Furthermore, a new mechanism for NF-kappaB downregulation is emerging that involves the degradation of active NF-kappaB by the nuclear ubiquitin-proteasome system. Here we review new aspects of NF-kappaB and IRF regulation chiefly in DCs.

PMID:
18534908
DOI:
10.1016/j.it.2008.03.005
[Indexed for MEDLINE]

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