The AIM 2 inflammasome: Sensor of pathogens and cellular perturbations
Open accessAbstract
Summary: Recognition of pathogens and altered self must be efficient and highly specific to orchestrate appropriate responses while limiting excessive inflammation and autoimmune reaction to normal self. AIM 2 is a member of innate immune sensors that detects the presence of DNA, arguably the most conserved molecules in living organisms. However, AIM 2 achieves specificity by detecting altered or mislocalized DNA molecules. It can detect damaged DNA, and the aberrant presence of DNA within the cytosolic compartment such as genomic DNA released into the cytosol upon loss of nuclear envelope integrity. AIM 2 is also a key sensor of pathogens that detects the presence of foreign DNA accumulating in the cytosol during the life cycle of intracellular pathogens including viruses, bacteria, and parasites. AIM 2 activation initiates the assembly of the inflammasome, an innate immune complex that leads to the activation of inflammatory caspases. This triggers the maturation and secretion of the cytokines IL‐1β and IL‐18. It can also initiate pyroptosis, a proinflammatory form of cell death. The AIM 2 inflammasome contributes to physiological responses and diseases. It is a key player in host defenses, but its deregulation can contribute immune‐linked diseases, such as autoinflammatory and autoimmune pathologies. Moreover, AIM 2 may play a role in cancer development. Recent studies have shown that the detection of self‐DNA species by AIM 2 is an important factor that contributes to diseases associated with perturbation of cellular homeostasis. Thus, in addition of being a sensor of pathogen associated molecular patterns (PAMP s), the AIM 2 inflammasome is emerging as a key guardian of cellular integrity.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
cGAS is a cytosolic dsDNA sensor associated with STING, and AIM2 is a cytosolic dsDNA sensor whose activation leads to inflammasome assembly.
“Two sensors capable of recognizing double-stranded (ds)DNA and which are found, crucially, in the cytosol are cyclic GMP-AMP synthase (cGAS), an enzyme associated with downstream adaptor molecule stimulator of interferon (STING), and absent in melanoma 2 (AIM2), whose activation leads to the assembly of a multi-protein complex stimulating inflammatory caspases called the inflammasome [79,80].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [80]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 168 · Cited by 333
Research works printed but not linked: 2
- [3]3. Gay NJ, Symmons MF, Gangloff M, Bryant CE. Assembly and localization of Tolllike receptor signalling complexes. Nature reviews Immunology.2014;14:546-558.
- [5]5. Ludlow LE, Johnstone RW, Clarke CJ. The HIN-200 family: more than interferoninducible genes? Experimental cell research.2005;308:1-17.
- Authors
- Lugrin, J., & Martinon, F.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- University of Lausanne (CH)
- Corresponding author
- Martinon, Fabio
- Venue
- Immunological Reviews
- Publisher
- Wiley
- Published
- 2017-12-16
- Volume
- 281
- Issue
- 1
- Pages
- 99-114
- ISSN
- 0105-2896 (ISSN-L)
- 1600-065X
- OpenAlex
- W2773720435
- Cited by
- 333
- References
- 168
- Citations by year
- 2026: 16 · 2025: 30 · 2024: 46 · 2023: 48 · 2022: 48 · 2021: 40 · 2020: 52 · 2019: 34 · 2018: 18 · 2017: 1
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- green
- serval.unil.ch
- Licence
- Locations
- Immunological Reviews (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- IRIS (submittedVersion)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (310030_173152)
- 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 › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- AIM2 inflammasome, innate immune sensors, cytosolic DNA sensing, self-DNA, pathogen-associated molecular patterns, pyroptosis, IL-1β, IL-18, inflammatory caspases, autoinflammatory disease, autoimmune disease, cancer, nuclear envelope integrity, intracellular pathogens
- MeSH terms
- Pathogen-Associated Molecular Pattern Molecules, Animals, DNA, DNA Damage, DNA-Binding Proteins, Homeostasis, Humans, Immunity, Innate, Cell Death, Caspases, Host-Pathogen Interactions, Inflammasomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review