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Immunity. 2012 Jul 27;37(1):96-107. doi: 10.1016/j.immuni.2012.07.006.

The NLRP12 inflammasome recognizes Yersinia pestis.

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  • 1Division of Infectious Diseases and Immunology, UMass Medical School, Worcester, MA 01605, USA.

Erratum in

  • Immunity. 2012 Sep 21;37(3):588.

Abstract

Yersinia pestis, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1β, which are generated through caspase-1-activating nucleotide-binding domain and leucine-rich repeat (NLR)-containing inflammasomes. Here, we sought to elucidate the role of NLRs and IL-18 during plague. Lack of IL-18 signaling led to increased susceptibility to Y. pestis, producing tetra-acylated lipid A, and an attenuated strain producing a Y. pseudotuberculosis-like hexa-acylated lipid A. We found that the NLRP12 inflammasome was an important regulator controlling IL-18 and IL-1β production after Y. pestis infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-γ production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-κB. These studies reveal a role for NLRP12 in host resistance against pathogens. Minimizing NLRP12 inflammasome activation may have been a central factor in evolution of the high virulence of Y. pestis.

Copyright © 2012 Elsevier Inc. All rights reserved.

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