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Lisa Waggoner

Researcher at University of Massachusetts Medical School

Publications -  8
Citations -  1996

Lisa Waggoner is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Inflammasome & Innate immune system. The author has an hindex of 6, co-authored 7 publications receiving 1796 citations.

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The AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses.

TL;DR: A central role is identified in regulating caspase-1-dependent maturation of IL-1β and IL-18, as well as pyroptosis, in response to synthetic double-stranded DNA, demonstrating the importance of AIM2 in the sensing of both bacterial and viral pathogens and in triggering innate immunity.
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TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.

TL;DR: The identification of TRIF as a regulator of caspase-11 underscores the importance of TLRs as master regulators of inflammasomes during Gram-negative bacterial infection.
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Allergens as Immunomodulatory Proteins: The Cat Dander Protein Fel d 1 Enhances TLR Activation by Lipid Ligands

TL;DR: It is proposed that Fel d 1 and Can f 6 belong to a group of allergen immunomodulatory proteins that enhance innate immune signaling and promote airway hypersensitivity reactions in diseases such as asthma.
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TRIM13 Is a Negative Regulator of MDA5-Mediated Type I Interferon Production

TL;DR: It is demonstrated that expression of the gene tripartite motif 13 (Trim13) is upregulated in response to inducers of type I IFN and that TRIM13 interacts with both MDA5 and RIG-I in vitro, which places it at a key junction within the viral response pathway.
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O008 Type I interferons license caspase-11-dependent NLRP3 inflammasome activation by Gram-negative bacteria

TL;DR: The identification of type I interferon as a regulator of caspase-11-dependent NLRP3 inflammasome activation provides new insights into the integration of TLR and NLR pathways during Gram-negative bacterial infections and unveils new targets that might be manipulated to prevent uncontrolled inflammation during septic shock.