Cellular signaling, molecular activation, and regulation of the AIM2 inflammasome

Lozano-Ruiz, Beatriz; Tzoumpa, Amalia; Picó, Joanna; Yin, Hao; González‐Navajas, José M.

doi:10.1016/b978-0-323-91802-2.00027-x

Cited by 3 publications

(7 citation statements)

References 83 publications

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“…ALRs are coded by four genes (in humans): AIM2, interferon gamma inducible protein 16 (IFI16), pyrin and HIN domain family member 1 (PYHIN1) and myeloid cell nuclear differentiation antigen (MNDA) (Brunette et al., 2012). In structural terms, ALRs consist of two main domains: a pyrin domain (PYD) and a haematopoietic expression, interferon inducible and nuclear localization with 200 amino acid repeat (HIN‐200) domain (Lozano‐Ruiz et al., 2023). Instead, NLRs are a superfamily of cytoplasmic PRRs; in humans they contain four characterized subfamily members: NLR family acidic domain containing (NLRA), NLR family BIR domain containing (NLRB), NLR family CARD domain containing (NLRC) and NLR family pyrin domain containing (NLRP) as well as NLR family member X (NLRX), which lacks a fully characterized N‐terminal domain (Hochheiser & Geyer, 2023; Ting et al., 2008).…”

Section: Review Of the Literaturementioning

confidence: 99%

Inflammasome activation in response to aberrations of cellular homeostasis in epithelial cells from human cornea and retina

Korhonen

2024

Acta Ophthalmologica

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Section: Review Of the Literaturementioning

confidence: 99%

Inflammasome activation in response to aberrations of cellular homeostasis in epithelial cells from human cornea and retina

Korhonen

2024

Acta Ophthalmologica

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“…Activation of Inflammasome by AIM2 is responsible for IL-1β release following infection from various DNA viruses such as vaccinia virus and adenovirus. 38,40 NLRP1 can identify anthrax lethal toxin (ALT) and NLRP3 recognizes bacterial toxins, especially various proteins of IV and other stimuli such as ATP. DNA and IV infections are recognized by the AIM2 receptor.…”

Section: Interconnection Of Panoptosis Innate Immune Responses and In...mentioning

confidence: 99%

“…As well, binding of DNA to AIM2 induces its oligomerization and recruitment of ASC through its pyrin domain, resulting in activation of caspase 1 as in the case of the NLRs. Activation of Inflammasome by AIM2 is responsible for IL‐1β release following infection from various DNA viruses such as vaccinia virus and adenovirus 38,40 …”

Section: Interconnection Of Panoptosis Innate Immune Responses and In...mentioning

confidence: 99%

“…In addition, NLRP6, 9, and 12, PIRYN, and other inflammasome receptors are observed to initiate inflammasome assembly. Inflammasomes are the common defense mechanism in MQs, NE, and DCs as innate immune cells 38,40,41 …”

Section: Interconnection Of Panoptosis Innate Immune Responses and In...mentioning

confidence: 99%

“…Inflammasomes are the common defense mechanism in MQs, NE, and DCs as innate immune cells. 38,40,41 Further, NLRs, RLRs, and TLRs, as PRRs family, are identified to cooperate for early detection of IvA and induce host responses which are regarded as protective, aid in removing infection, and can promote disease burden when responses are considered as further and prolonged. HA, as an IvA glycoprotein, can attach to sialic acid expressed by a cell surface receptor.…”

Section: Interconnection Of Panoptosis Innate Immune Responses and In...mentioning

confidence: 99%

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Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review

Wei,

Wang,

Zhou

2023

Immunity Inflam & Disease

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BackgroundInfluenza virus (IV) is a leading cause of respiratory tract infections, eliciting responses from key innate immune cells such as Macrophages (MQs), Neutrophils, and Dendritic Cells (DCs). These cells employ diverse mechanisms to combat IV, with Inflammasomes playing a pivotal role in viral infection control. Cellular death mechanisms, including Pyroptosis, Apoptosis, and Necroptosis (collectively called PANoptosis), significantly contribute to the innate immune response.MethodsIn this updated review, we delve into the intricate relationship between PANoptosis and Inflammasomes within innate immune cells (MQs, Neutrophils, and DCs) during IV infections. We explore the strategies employed by IV to evade these immune defenses and the consequences of unchecked PANoptosis and inflammasome activation, including the potential development of severe complications such as cytokine storms and tissue damage.ResultsOur analysis underscores the interplay between PANoptosis and Inflammasomes as a critical aspect of the innate immune response against IV. We provide insights into IV's various mechanisms to subvert these immune pathways and highlight the importance of understanding these interactions to develop effective antiviral medications.ConclusionA comprehensive understanding of the dynamic interactions between PANoptosis, Inflammasomes, and IV is essential for advancing our knowledge of innate immune responses to viral infections. This knowledge will be invaluable in developing targeted antiviral therapies to combat IV and mitigate potential complications, including cytokine storms and tissue damage.

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Inflammasome activity regulation by PUFA metabolites

Atalay Ekiner,

Gęgotek,

Skrzydlewska

2024

Front. Immunol.

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Oxidative stress and the accompanying chronic inflammation constitute an important metabolic problem that may lead to pathology, especially when the body is exposed to physicochemical and biological factors, including UV radiation, pathogens, drugs, as well as endogenous metabolic disorders. The cellular response is associated, among others, with changes in lipid metabolism, mainly due to the oxidation and the action of lipolytic enzymes. Products of oxidative fragmentation/cyclization of polyunsaturated fatty acids (PUFAs) [4-HNE, MDA, 8-isoprostanes, neuroprostanes] and eicosanoids generated as a result of the enzymatic metabolism of PUFAs significantly modify cellular metabolism, including inflammation and the functioning of the immune system by interfering with intracellular molecular signaling. The key regulators of inflammation, the effectiveness of which can be regulated by interacting with the products of lipid metabolism under oxidative stress, are inflammasome complexes. An example is both negative or positive regulation of NLRP3 inflammasome activity by 4-HNE depending on the severity of oxidative stress. 4-HNE modifies NLRP3 activity by both direct interaction with NLRP3 and alteration of NF-κB signaling. Furthermore, prostaglandin E2 is known to be positively correlated with both NLRP3 and NLRC4 activity, while its potential interference with AIM2 or NLRP1 activity is unproven. Therefore, the influence of PUFA metabolites on the activity of well-characterized inflammasome complexes is reviewed.

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Cellular signaling, molecular activation, and regulation of the AIM2 inflammasome

Cited by 3 publications

References 83 publications

Inflammasome activation in response to aberrations of cellular homeostasis in epithelial cells from human cornea and retina

Inflammasome activation in response to aberrations of cellular homeostasis in epithelial cells from human cornea and retina

Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review

Inflammasome activity regulation by PUFA metabolites

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