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Review
. 2012 Sep;92(3):469-77.
doi: 10.1189/jlb.0312132. Epub 2012 May 10.

NLRs, inflammasomes, and viral infection

Sarah R Jacobs  1 , Blossom Damania
Affiliations
Review

NLRs, inflammasomes, and viral infection

Sarah R Jacobs et al. J Leukoc Biol. 2012 Sep.

Erratum in

  • J Leukoc Biol. 2012 Nov;92(5):1123

Abstract

NLR proteins are innate immune sensors that respond to microbial infection. Upon pathogen infection, some NLR proteins form large complexes, called inflammasomes, which activate caspase-1 and induce the production of active IL-1β and IL-18. Activation of inflammasomes can also lead to an inflammatory cell death program, named pyroptosis. In this review, we will discuss the role of various NLR proteins in sensing different viral infections, as well as the strategies used by several RNA and DNA viruses to counteract the antiviral effects of NLR-dependent inflammasomes.

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Figures

Figure 1.
Figure 1.. Viral proteins inhibit various steps of the NLR-dependent inflammasome pathway.
Some poxviruses encode scavenger receptors (vIL-1βR) and IL-18BPs, which compete with IL-1β and IL-18 from binding their cognate receptors. Moreover, MxV and Shope fibroma virus encode vPOPs, which bind ASC to prevent inflammasome formation through caspase-1 recruitment. Measles virus encodes a nonstructural V protein that interacts with and inhibits NLRP3. Similarly, KSHV encodes the Orf63 protein, which shows similarity to cellular NLRP1 and can interact with cellular NLRP1 and NLRP3 to prevent the formation of inflammasomes. Poxvirus family members encode serpins such as CrmA, SP1/2 (SPI-1/2), and Serp2, which inhibit caspase-1 activity and prevent IL-1β and IL-18 secretion. The NS1 protein of influenza also inhibits caspase-1, IL-1β, and IL-18 activation and secretion. HMGB1, High mobility group box 1.
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References

    1. Kawai T., Akira S. (2008) Toll-like receptor and RIG-I-like receptor signaling. Ann. N. Y. Acad. Sci. 1143, 1–20 - PubMed
    1. Bianchi M. E. (2007) DAMPs, PAMPs and alarmins: all we need to know about danger. J. Leukoc. Biol. 81, 1–5 - PubMed
    1. Medzhitov R., Preston-Hurlburt P., Janeway C. A., Jr., (1997) A human homologue of the Drosophila Toll protein signals activation of adaptive immunity. Nature 388, 394–397 - PubMed
    1. Leulier F., Lemaitre B. (2008) Toll-like receptors—taking an evolutionary approach. Nat. Rev. Genet. 9, 165–178 - PubMed
    1. Kawai T., Akira S. (2007) TLR signaling. Sem. Immunol. 19, 24–32 - PubMed

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