| Literature DB >> 27460808 |
Erin Theisen1, John-Demian Sauer2.
Abstract
Inflammasomes are cytosolic innate immune surveillance systems that recognize a variety of danger signals, including those from pathogens. Listeria monocytogenes is a Gram-positive intracellular bacterium evolved to live within the harsh environment of the host cytosol. Further, L. monocytogenes can activate a robust cell-mediated immune response that is being harnessed as an immunotherapeutic platform. Access to the cytosol is critical for both causing disease and inducing a protective immune response, and it is hypothesized that the cytosolic innate immune system, including the inflammasome, is critical for both host protection and induction of long-term immunity. L. monocytogenes can activate a variety of inflammasomes via its pore-forming toxin listeriolysin-O, flagellin, or DNA released through bacteriolysis; however, inflammasome activation attenuates L. monocytogenes, and as such, L. monocytogenes has evolved a variety of ways to limit inflammasome activation. Surprisingly, inflammasome activation also impairs the host cell-mediated immune response. Thus, understanding how L. monocytogenes activates or avoids detection by the inflammasome is critical to understand the pathogenesis of L. monocytogenes and improve the cell-mediated immune response generated to L. monocytogenes for more effective immunotherapies.Entities:
Keywords: AIM2; Adaptive immunity; Immunotherapy; Inflammasome; Innate immunity macrophage; Listeria monocytogenes
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Year: 2016 PMID: 27460808 PMCID: PMC5027901 DOI: 10.1007/978-3-319-41171-2_7
Source DB: PubMed Journal: Curr Top Microbiol Immunol ISSN: 0070-217X Impact factor: 4.291