The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
The AIM2 inflammasome is critical for innate immunity to Francisella tularensis
Open accessAbstract
Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F. tularensis and elicit this proinflammatory response. Using mice deficient in the DNA-sensing inflammasome component AIM2, we demonstrate here that AIM2 is required for sensing F. tularensis. AIM2-deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bacterial burden than that of wild-type mice. Caspase-1 activation, IL-1beta secretion and cell death were absent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic DNA. Our study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of its critical role in host innate immunity to intracellular pathogens.
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“AIM2 has a demonstrated role in immune responses directed against both bacteria51 and DNA viruses52, but it will be important to determine whether there is a physiological role for AIM2 in sterile inflammation, especially in autoimmune diseases such as systemic lupus erythematosus, which is associated with elevated circulating levels of dsDNA.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [51]
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Cites
Pathogen Recognition and Innate Immunity
Akira, S., Uematsu, S., & Takeuchi, O. (2006) · Cell · doi:10.1016/j.cell.2006.02.015 · Cited by 11,976
Bauernfeind, F. G., Horvath, G. L., Stutz, A., Alnemri, E. S., MacDonald, K. L., Speert, D. P., Fernandes‐Alnemri, T., Wu, J., Monks, B. G., Fitzgerald, K. A., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901363 · Cited by 3,087
Self-citationCryopyrin activates the inflammasome in response to toxins and ATP
Mariathasan, S., Weiss, D. S., Newton, K., McBride, J., O'Rourke, K., Roose-Girma, M., Lee, W. P., Weinrauch, Y., Monack, D. M., & Dixit, V. M. (2006) · Nature · doi:10.1038/nature04515 · Cited by 3,080
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AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC
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The NALP3 inflammasome is involved in the innate immune response to amyloid-β
Halle, A., Hornung, V., Petzold, G. C., Stewart, C. R., Monks, B. G., Reinheckel, T., Fitzgerald, K. A., Latz, E., Moore, K. J., & Golenbock, D. T. (2008) · Nature Immunology · doi:10.1038/ni.1636 · Cited by 2,441
The Inflammasomes: Guardians of the Body
Martinon, F., Mayor, A., & Tschopp, J. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132715 · Cited by 2,436
Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf
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AIM2 activates the inflammasome and cell death in response to cytoplasmic DNA
Fernandes-Alnemri, T., Yu, J.-W., Datta, P., Wu, J., & Alnemri, E. S. (2009) · Nature · doi:10.1038/nature07710 · Cited by 1,831
Self-citationFranchi, L., Amer, A., Body-Malapel, M., Kanneganti, T.-D., Özören, N., Jagirdar, R., Inohara, N., Vandenabeele, P., Bertin, J., Coyle, A., et al. (2006) · Nature Immunology · doi:10.1038/ni1346 · Cited by 1,131
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Metadata
- Authors
- Fernandes-Alnemri, T., Yu, J.-W., Juliana, C., Solorzano, L., Kang, S., Wu, J., Datta, P., McCormick, M., Huang, L., McDermott, E., Eisenlohr, L., Landel, C. P., & Alnemri, E. S.
- Affiliations
- Thomas Jefferson University (US)
- Corresponding author
- Alnemri, Emad S
- Venue
- Nature Immunology
- Published
- 2010-03-28
- Volume
- 11
- Issue
- 5
- Pages
- 385-393
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC3111085
- OpenAlex
- W2157305255
- Cited by
- 732
- References
- 45
- Citations by year
- 2026: 26 · 2025: 19 · 2024: 34 · 2023: 22 · 2022: 25 · 2021: 35 · 2020: 30 · 2019: 39 · 2018: 42 · 2017: 60 · 2016: 53 · 2015: 57 · 2014: 58 · 2013: 73 · 2012: 51
- FWCI
- 29.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Harvard University
- National Institutes of Health
- National Institute on Aging (AG14357, R01AG014357)
- National Cancer Institute (T32 CA09678, T32CA009678)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-055398, R01AR055398)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacillus and Francisella bacterial research
- Keywords
- AIM2 inflammasome, Francisella tularensis, tularemia, innate immunity, macrophages, cytosolic DNA sensing, caspase-1 activation, IL-1β, IL-18, intracellular bacterial infection, host defense
- MeSH terms
- Animals, Cells, Cultured, DNA-Binding Proteins, Francisella tularensis, Humans, Immunity, Innate, Interferon Type I, L-Lactate Dehydrogenase, Macrophages, Nuclear Proteins, Tularemia, Mice, Knockout, Calcium Signaling, Caspase 1, Multiprotein Complexes, Interferon Regulatory Factor-3, Mice, Interleukin-1beta, Protein Multimerization
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