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3. NLRC5 negatively regulates the NF-kappaB and type I interferon signaling pathways.

Author

Cui J, Zhu L, Xia X, Wang HY, Legras X, Hong J, Ji J, Shen P, Zheng S, Chen ZJ, and Wang RF

Subjects
Animals, Cloning, Molecular, DEAD-box RNA Helicases metabolism, Humans, I-kappa B Kinase metabolism, Inflammation, Intracellular Signaling Peptides and Proteins chemistry, Ligands, Mice, Phosphorylation, Toll-Like Receptors metabolism, Immunity, Innate, Interferon Type I metabolism, Intracellular Signaling Peptides and Proteins metabolism, NF-kappa B metabolism, Signal Transduction
Abstract

Stringent control of the NF-kappaB and type I interferon signaling pathways is critical to effective host immune responses, yet the molecular mechanisms that negatively regulate these pathways are poorly understood. Here, we show that NLRC5, a member of the highly conserved NOD-like protein family, can inhibit the IKK complex and RIG-I/MDA5 function. NLRC5 inhibited NF-kappaB-dependent responses by interacting with IKKalpha and IKKbeta and blocking their phosphorylation. It also interacted with RIG-I and MDA5, but not with MAVS, to inhibit RLR-mediated type I interferon responses. Consistent with these observations, NLRC5-specific siRNA knockdown not only enhanced the activation of NF-kappaB and its responsive genes, TNF-alpha and IL-6, but also promoted type I interferon signaling and antiviral immunity. Our findings identify NLRC5 as a negative regulator that blocks two central components of the NF-kappaB and type I interferon signaling pathways and suggest an important role for NLRC5 in homeostatic control of innate immunity., (2010 Elsevier Inc. All rights reserved.)

Published
2010
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