Abstract
Abstract Recognition of pathogens by the cell is paramount for the initiation of an appropriate immune response. A subset of pattern-recognition receptor family, including NLRP3, NLRC4 and AIM2, are cytosolic sensors which induce formation of the inflammasome, a multi-protein complex which drives the release of the pro-inflammatory cytokines IL-1β and IL-18. Here, we found that guanylate-binding proteins and other novel interferon-inducible GTPases were required for activation of the DNA-sensing AIM2 inflammasome during infection with Francisella novicida. These proteins were recruited to the cell membrane of the bacteria to mediate bacteriolysis, and thereby, liberating DNA for sensing by AIM2. However, engagement of the AIM2 inflammasome by mouse cytomegalovirus or transfected double-stranded DNA did not require interferon-inducible GTPases. Our results reveal a specific mechanistic link between cell-autonomous immunity and innate immune sensing pathways in response to bacterial infection.
Published Version
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