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  1. Article ; Online: Ten things to know about NLRP10.

    Masters, Seth L

    Nature immunology

    2023  Volume 24, Issue 4, Page(s) 561–562

    MeSH term(s) Adaptor Proteins, Signal Transducing ; Carrier Proteins
    Chemical Substances Adaptor Proteins, Signal Transducing ; Carrier Proteins
    Language English
    Publishing date 2023-03-05
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01466-5
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  2. Book ; Online ; Thesis: From pattern recognition to pro-inflammatory cell death - Functional characterization of the proteins NLRP7 and GSDMD

    Kopp, Anja [Verfasser] / Geyer, Matthias [Akademischer Betreuer] / Masters, Seth L. [Gutachter]

    2023  

    Author's details Anja Kopp ; Gutachter: Seth L. Masters ; Betreuer: Matthias Geyer
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language English
    Publisher Universitäts- und Landesbibliothek Bonn
    Publishing place Bonn
    Document type Book ; Online ; Thesis
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  3. Article ; Online: Broadening the definition of autoinflammation.

    Masters, Seth L

    Seminars in immunopathology

    2015  Volume 37, Issue 4, Page(s) 311–312

    Abstract: Initially, the concept of autoinflammation posited that there be no involvement of autoreactive B or T cells, and no evidence of infection. These criteria served well to help establish the concept, and distinguish autoinflammatory diseases from ... ...

    Abstract Initially, the concept of autoinflammation posited that there be no involvement of autoreactive B or T cells, and no evidence of infection. These criteria served well to help establish the concept, and distinguish autoinflammatory diseases from autoimmune or infectious conditions. However, the characterisation of additional monogenic autoinflammatory diseases has established that a primary trigger of the innate immune system may also be accompanied by infection or manifestations of autoimmunity, which may even contribute to pathogenesis. This issue of Seminars in Immunopathology draws out these themes and also shows how autoinflammation can help to maintain homeostasis, which is its primary evolutionary function. Elucidating the fundamental innate immune pathways underlying autoinflammatory disease leads back to these same homeostatic parameters, to inform about how infection is sensed, and providing for new targets against chronic inflammatory disease.
    MeSH term(s) Autoimmune Diseases/diagnosis ; Autoimmune Diseases/etiology ; Hereditary Autoinflammatory Diseases/diagnosis ; Hereditary Autoinflammatory Diseases/etiology ; Humans ; Inflammation/diagnosis ; Inflammation/etiology
    Language English
    Publishing date 2015-07
    Publishing country Germany
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-015-0497-1
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  4. Article ; Online: Caspase substrates won't be defined by a four-letter code.

    Baker, Paul J / Masters, Seth L

    The Journal of biological chemistry

    2018  Volume 293, Issue 18, Page(s) 7068–7069

    Abstract: Inflammatory cell death can be mediated by the murine caspase-1 and -11. Genetic and cell biological data point to conflicting conclusions whether these caspases cleave the same substrates or use distinct mechanisms to mediate inflammation and cell death. ...

    Abstract Inflammatory cell death can be mediated by the murine caspase-1 and -11. Genetic and cell biological data point to conflicting conclusions whether these caspases cleave the same substrates or use distinct mechanisms to mediate inflammation and cell death. Peptide screening and biochemical analysis by Gonzales Ramirez
    MeSH term(s) Animals ; Caspase 1 ; Caspases ; Cell Death ; Mice ; Peptides ; Substrate Specificity
    Chemical Substances Peptides ; Caspases (EC 3.4.22.-) ; Caspase 1 (EC 3.4.22.36)
    Language English
    Publishing date 2018-09-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.H118.002802
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  5. Article ; Online: The classification, genetic diagnosis and modelling of monogenic autoinflammatory disorders.

    Moghaddas, Fiona / Masters, Seth L

    Clinical science (London, England : 1979)

    2018  Volume 132, Issue 17, Page(s) 1901–1924

    Abstract: Monogenic autoinflammatory disorders are an increasingly heterogeneous group of conditions characterised by innate immune dysregulation. Improved genetic sequencing in recent years has led not only to the discovery of a plethora of conditions considered ... ...

    Abstract Monogenic autoinflammatory disorders are an increasingly heterogeneous group of conditions characterised by innate immune dysregulation. Improved genetic sequencing in recent years has led not only to the discovery of a plethora of conditions considered to be 'autoinflammatory', but also the broadening of the clinical and immunological phenotypic spectra seen in these disorders. This review outlines the classification strategies that have been employed for monogenic autoinflammatory disorders to date, including the primary innate immune pathway or the dominant cytokine implicated in disease pathogenesis, and highlights some of the advantages of these models. Furthermore, the use of the term 'autoinflammatory' is discussed in relation to disorders that cross the innate and adaptive immune divide. The utilisation of next-generation sequencing (NGS) in this population is examined, as are potential
    MeSH term(s) Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Genetic Association Studies ; Genetic Predisposition to Disease/genetics ; Hereditary Autoinflammatory Diseases/classification ; Hereditary Autoinflammatory Diseases/genetics ; Hereditary Autoinflammatory Diseases/immunology ; Humans ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Inflammasomes/genetics ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Mutation
    Chemical Substances Cytokines ; Inflammasomes
    Language English
    Publishing date 2018-09-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20171498
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  6. Article ; Online: The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration.

    Jackson, Jacob T / Mulazzani, Elisabeth / Nutt, Stephen L / Masters, Seth L

    The Journal of biological chemistry

    2021  Volume 297, Issue 2, Page(s) 100905

    Abstract: Phosphatidylinositol-specific phospholipase Cγ2 (PLCγ2) is a critical signaling molecule activated downstream from a variety of cell surface receptors that contain an intracellular immunoreceptor tyrosine-based activation motif. These receptors recruit ... ...

    Abstract Phosphatidylinositol-specific phospholipase Cγ2 (PLCγ2) is a critical signaling molecule activated downstream from a variety of cell surface receptors that contain an intracellular immunoreceptor tyrosine-based activation motif. These receptors recruit kinases such as Syk, BTK, and BLNK to phosphorylate and activate PLCγ2, which then generates 1D-myo-inositol 1,4,5-trisphosphate and diacylglycerol. These well-known second messengers are required for diverse membrane functionality including cellular proliferation, endocytosis, and calcium flux. As a result, PLCγ2 dysfunction is associated with a variety of diseases including cancer, neurodegeneration, and immune disorders. The diverse pathologies associated with PLCγ2 are exemplified by distinct genetic variants. Inherited mutations at this locus cause PLCγ2-associated antibody deficiency and immune dysregulation, in some cases with autoinflammation. Acquired mutations at this locus, which often arise as a result of BTK inhibition to treat chronic lymphocytic leukemia, result in constitutive downstream signaling and lymphocyte proliferation. Finally, a third group of PLCγ2 variants actually has a protective effect in a variety of neurodegenerative disorders, presumably by increased uptake and degradation of deleterious neurological aggregates. Therefore, manipulating PLCγ2 activity either up or down could have therapeutic benefit; however, we require a better understanding of the signaling pathways propagated by these variants before such clinical utility can be realized. Here, we review the signaling roles of PLCγ2 in hematopoietic cells to help understand the effect of mutations driving immune disorders and cancer and extrapolate from this to roles which may relate to protection against neurodegeneration.
    MeSH term(s) Agammaglobulinaemia Tyrosine Kinase/immunology ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Animals ; Calcium Signaling ; Humans ; Immune System Diseases/genetics ; Immune System Diseases/immunology ; Immune System Diseases/metabolism ; Immune System Diseases/pathology ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/immunology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Phospholipase C gamma/genetics ; Phospholipase C gamma/immunology ; Phospholipase C gamma/metabolism ; Syk Kinase/immunology ; Syk Kinase/metabolism
    Chemical Substances Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Syk Kinase (EC 2.7.10.2) ; PLCG2 protein, human (EC 3.1.4.3) ; Phospholipase C gamma (EC 3.1.4.3)
    Language English
    Publishing date 2021-06-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2021.100905
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  7. Article ; Online: Pyrin variant E148Q potentiates inflammasome activation and the effect of pathogenic mutations in cis.

    Reygaerts, Thomas / Laohamonthonkul, Pawat / Hrovat-Schaale, Katja / Moghaddas, Fiona / Baker, Paul J / Gray, Paul E / Masters, Seth L

    Rheumatology (Oxford, England)

    2023  Volume 63, Issue 3, Page(s) 882–890

    Abstract: Objective: The p.E148Q variant in pyrin is present in different populations at a frequency of up to 29%, and has been associated with diseases, including vasculitis and FMF. The pathogenicity of p.E148Q in FMF is unclear, even when observed in cis or in ...

    Abstract Objective: The p.E148Q variant in pyrin is present in different populations at a frequency of up to 29%, and has been associated with diseases, including vasculitis and FMF. The pathogenicity of p.E148Q in FMF is unclear, even when observed in cis or in trans to a single, typically recessive, pathogenic mutation. We performed functional validation to determine whether p.E148Q increases the ability of pyrin to form an active inflammasome complex in cell lines.
    Methods: We interrogated the Australian Autoinflammatory Disease RegistrY (AADRY) to find candidate inheritance patterns for the p.E148Q variant in pyrin. Different pyrin variant combinations were tested in HEK293T cells stably expressing the adaptor protein apoptosis-associated speck-like (ASC), which were analysed by flow cytometry to visualize inflammasome formation, with and without stimulation by Clostridioides difficile toxin B (TcdB). Inflammasome-dependent cytokine secretion was also quantified by ELISA of supernatants from THP-1 cells transduced with lentiviral expression vectors.
    Results: In AADRY, we observed the p.E148Q allele in individuals with autoinflammatory diseases alone or in conjunction with other pyrin variants. Two FMF families harboured the allele p.E148Q-M694I in cis with dominant heritability. In vitro, p.E148Q pyrin could spontaneously potentiate inflammasome formation, with increased IL-1β and IL-18 secretion. p.E148Q in cis to classical FMF mutations provided significant potentiation of inflammasome formation.
    Conclusion: The p.E148Q variant in pyrin potentiates inflammasome activation in vitro. In cis, this effect is additive to known pathogenic FMF mutations. In some families, this increased effect could explain why FMF segregates as an apparently dominant disease.
    MeSH term(s) Humans ; Australia ; Bacterial Toxins/pharmacology ; HEK293 Cells ; Inflammasomes/genetics ; Mutation ; Pyrin/genetics
    Chemical Substances Bacterial Toxins ; Inflammasomes ; Pyrin ; toxB protein, Clostridium difficile
    Language English
    Publishing date 2023-07-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 1464822-2
    ISSN 1462-0332 ; 1462-0324
    ISSN (online) 1462-0332
    ISSN 1462-0324
    DOI 10.1093/rheumatology/kead376
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  8. Article ; Online: Generation of Genetic Knockouts in Myeloid Cell Lines Using a Lentiviral CRISPR/Cas9 System.

    Baker, Paul J / Masters, Seth L

    Methods in molecular biology (Clifton, N.J.)

    2017  Volume 1714, Page(s) 41–55

    Abstract: CRISPR/Cas9-based gene targeting allows deletion of a gene of interest from cultured cell lines. Due to difficulty in transiently transfecting hematopoetic cells with components required for this process, we have adopted a lentiviral system for delivery ... ...

    Abstract CRISPR/Cas9-based gene targeting allows deletion of a gene of interest from cultured cell lines. Due to difficulty in transiently transfecting hematopoetic cells with components required for this process, we have adopted a lentiviral system for delivery of the CRISPR/Cas9 components into myeloid cell lines. Here, we detail the process of knocking out genes from pools of cultured myeloid cells using this CRISPR/Cas9 system and describe methods of validating these knockout pools.
    MeSH term(s) Animals ; CRISPR-Cas Systems ; Cells, Cultured ; Gene Knockout Techniques/methods ; Genetic Vectors ; Humans ; Lentivirus/genetics ; Mice ; Myeloid Cells/cytology ; Myeloid Cells/metabolism
    Language English
    Publishing date 2017-11-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-7519-8_3
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  9. Article ; Online: Specific inflammasomes in complex diseases.

    Masters, Seth L

    Clinical immunology (Orlando, Fla.)

    2013  Volume 147, Issue 3, Page(s) 223–228

    Abstract: Blocking the cytokines Interleukin-1beta (IL-1β) and Interleukin-18 (IL-18) benefits a diverse range of inflammatory pathologies. In each of these diseases, different cytoplasmic innate immune receptors nucleate individual protein complexes known as ... ...

    Abstract Blocking the cytokines Interleukin-1beta (IL-1β) and Interleukin-18 (IL-18) benefits a diverse range of inflammatory pathologies. In each of these diseases, different cytoplasmic innate immune receptors nucleate individual protein complexes known as inflammasomes, to regulate the production of active IL-1β or IL-18. This review will outline the complex diseases where these cytokines are pathogenic, and explain which inflammasome(s) may be responsible. For example, inflammasomes nucleated by NLRP3 and NLRP6 integrate signals from metabolic and commensal systems contributing to metabolic dysfunction and type 2 diabetes. On the other hand, NLRP1 and AIM2 are more broadly implicated in autoimmunity and allergy. Furthermore, each inflammasome has unique roles in pathogen recognition, which may determine the outcome of polymicrobial infection and link different infectious co-morbidities to chronic inflammatory disease. We can now imagine a time when targeted inflammasome inhibitors will be employed in the clinic, tailoring treatments to particular diseases, and perhaps individual patients.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Alzheimer Disease/genetics ; Alzheimer Disease/immunology ; Alzheimer Disease/metabolism ; Animals ; Apoptosis Regulatory Proteins/metabolism ; Atherosclerosis/genetics ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Carrier Proteins/metabolism ; DNA-Binding Proteins ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/metabolism ; Gout/genetics ; Gout/immunology ; Gout/metabolism ; Humans ; Inflammasomes/immunology ; Inflammatory Bowel Diseases/genetics ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/metabolism ; Interleukin-18/metabolism ; Interleukin-1beta/metabolism ; Intracellular Signaling Peptides and Proteins/immunology ; Intracellular Signaling Peptides and Proteins/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/immunology ; Obesity/genetics ; Obesity/immunology ; Obesity/metabolism
    Chemical Substances AIM2 protein, human ; Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; Carrier Proteins ; DNA-Binding Proteins ; Inflammasomes ; Interleukin-18 ; Interleukin-1beta ; Intracellular Signaling Peptides and Proteins ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP1 protein, human ; NLRP3 protein, human ; NLRP6 protein, human ; Nuclear Proteins
    Language English
    Publishing date 2013-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1459903-x
    ISSN 1521-7035 ; 1521-6616
    ISSN (online) 1521-7035
    ISSN 1521-6616
    DOI 10.1016/j.clim.2012.12.006
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  10. Article ; Online: Homeostasis-altering molecular processes as mechanisms of inflammasome activation.

    Liston, Adrian / Masters, Seth L

    Nature reviews. Immunology

    2017  Volume 17, Issue 3, Page(s) 208–214

    Abstract: The innate immune system uses a distinct set of germline-encoded pattern recognition receptors (PRRs) to initiate downstream inflammatory cascades. This recognition system is in stark contrast to the adaptive immune system, which relies on highly ... ...

    Abstract The innate immune system uses a distinct set of germline-encoded pattern recognition receptors (PRRs) to initiate downstream inflammatory cascades. This recognition system is in stark contrast to the adaptive immune system, which relies on highly variable, randomly generated antigen receptors. A key limitation of the innate immune system's reliance on fixed PRRs is its inflexibility in responding to rapidly evolving pathogens. Recent advances in our understanding of inflammasome activation suggest that the innate immune system also has sophisticated mechanisms for responding to pathogens for which there is no fixed PRR. This includes the recognition of debris from dying cells, known as danger-associated molecular patterns (DAMPs), which can directly activate PRRs in a similar manner to pathogen-associated molecular patterns (PAMPs). Distinct from this, emerging data for the inflammasome components NLRP3 (NOD-, LRR- and pyrin domain-containing 3) and pyrin suggest that they do not directly detect molecular patterns, but instead act as signal integrators that are capable of detecting perturbations in cytoplasmic homeostasis, for example, as initiated by infection. Monitoring these perturbations, which we term 'homeostasis-altering molecular processes' (HAMPs), provides potent flexibility in the capacity of the innate immune system to detect evolutionarily novel infections; however, HAMP sensing may also underlie the sterile inflammation that drives chronic inflammatory diseases.
    MeSH term(s) Animals ; Homeostasis/immunology ; Humans ; Immunity, Innate/immunology ; Inflammasomes/immunology ; Receptors, Pattern Recognition/immunology
    Chemical Substances Inflammasomes ; Receptors, Pattern Recognition
    Language English
    Publishing date 2017-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/nri.2016.151
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