ArticlemBio2022
Inflammasome Activation Dampens Type I IFN Signaling to Strengthen Anti-
Article in mBio, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- GBP5-triggered AIM2 inflammasome drives host defense and exacerbates disease severity during Neospora caninum infection.Veterinary research · 2026Article
- Luteolin Inhibits Bovine Viral Diarrhea Virus Replication by Disrupting Viral Internalization and Replication and Interfering with the NF-κB/STAT3-NLRP3 Inflammasome Pathway.Veterinary sciences · 2026Article
- Unraveling the role of host kinase PIM1 in Toxoplasma gondii infection: Implications for therapies.PLoS neglected tropical diseases · 2026Article
- Review
- Article
- Role of inflammasomes in Toxoplasma and Plasmodium infections.Parasites & vectors · 2024Review
- The Toxoplasma Effector GRA4 Hijacks Host TBK1 to Oppositely Regulate Anti-T. Gondii Immunity and Tumor Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A parasite odyssey: An RNA virus concealed inVirus evolution · 2024Article
- Vitamin D regulates COVID-19 associated severity by suppressing the NLRP3 inflammasome pathway.PloS one · 2024Article
- Mutual regulations betweenFrontiers in immunology · 2024Review
- Squaramides enhance NLRP3 inflammasome activation by lowering intracellular potassium.Cell death discovery · 2023Article
- New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases.Nutrients · 2023Review
- Article
- Capers with caspases: Toxoplasma gondii tales of inflammation and survival.Current opinion in microbiology · 2023Review
- Function and regulation of cGAS-STING signaling in infectious diseases.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immunity acts as the first line of defense against pathogen invasion. During Toxoplasma gondii infection, multiple innate immune sensors are activated by invading microbes or pathogen-associated molecular patterns (PAMPs). However, how inflammasome is activated and its regulatory mechanisms during T. gondii infection remain elusive. Here, we showed that the infection of PRU, a lethal type II T. gondii strain, activates inflammasome at the early stage of infection. PRU tachyzoites, RNA and soluble tachyzoite antigen (STAg) mainly triggered the NLRP3 inflammasome, while PRU genomic DNA (gDNA) specially activated the AIM2 inflammasome. Furthermore, mice deficient in AIM2, NLRP3, or caspase-1/11 were more susceptible to T. gondii PRU infection, and the ablation of inflammasome signaling impaired antitoxoplasmosis immune responses by enhancing type I interferon (IFN-I) production. Blockage of IFN-I receptor fulfilled inflammasome-deficient mice competent immune responses as WT mice. Moreover, we have identified that the suppressor of cytokine signaling 1 (SOCS1) is a key negative regulator induced by inflammasome-activated IL-1β signaling and inhibits IFN-I production by targeting interferon regulatory factor 3 (IRF3). In general, our study defines a novel protective role of inflammasome activation during toxoplasmosis and identifies a critical regulatory mechanism of the cross talk between inflammasome and IFN-I signaling for understanding infectious diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.