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  1. Book ; Online: CARMA Proteins: Playing a Hand of Four CARDs

    Bornancin, Frédéric / Snow, Andrew L.

    2019  

    Keywords Medicine ; Immunology ; CARD9 ; CARD10 ; CARD11 ; CARD14 ; CARMA proteins ; Lymphoma ; Psoriasis ; atopic disease ; Immunity ; immunodeficiency
    Size 1 electronic resource (179 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021231176
    ISBN 9782889630561 ; 2889630560
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book: Immune homeostasis

    Snow, Andrew L. / Lenardo, Michael J.

    methods and protocols

    (Methods in molecular biology ; 979 ; Springer protocols)

    2013  

    Author's details ed. by Andrew L. Snow
    Series title Methods in molecular biology ; 979
    Springer protocols
    Collection
    Language English
    Size XX, 450 S., Ill., graph. Darst.
    Publisher Humana Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT017568154
    ISBN 978-1-62703-289-6 ; 9781627032902 ; 1-62703-289-4 ; 1627032908
    Database Catalogue ZB MED Medicine, Health

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  3. Article ; Online: Epidermodysplasia Verruciformis in CADINS Disease: Expanding the Phenotype.

    Aggarwal, Ridhima / Spratt, Alison R / Snow, Andrew L / Vignesh, Pandiarajan

    Journal of clinical immunology

    2024  Volume 44, Issue 2, Page(s) 58

    MeSH term(s) Humans ; Epidermodysplasia Verruciformis/diagnosis ; Epidermodysplasia Verruciformis/genetics ; Phenotype
    Language English
    Publishing date 2024-02-05
    Publishing country Netherlands
    Document type Letter
    ZDB-ID 779361-3
    ISSN 1573-2592 ; 0271-9142
    ISSN (online) 1573-2592
    ISSN 0271-9142
    DOI 10.1007/s10875-024-01663-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mistuned NF-κB signaling in lymphocytes: lessons from relevant inborn errors of immunity.

    Dabbah-Krancher, Gina / Snow, Andrew L

    Clinical and experimental immunology

    2023  Volume 212, Issue 2, Page(s) 117–128

    Abstract: Inborn errors of immunity (IEIs) continuously remind us that multiple checks and balances are built into the adaptive immune system to maintain homeostasis, ensuring effective pathogen defense without causing inadvertent immunopathology, autoimmunity, or ...

    Abstract Inborn errors of immunity (IEIs) continuously remind us that multiple checks and balances are built into the adaptive immune system to maintain homeostasis, ensuring effective pathogen defense without causing inadvertent immunopathology, autoimmunity, or lymphomagenesis. The nuclear factor of κB (NF-κB) family of transcription factors serve a vital role in the immune system, inducing scores of genes responsible for lymphocyte survival, proliferation, differentiation and effector function. In recent years, the discovery and characterization of IEIs that impact NF-κB activity have illuminated the importance of carefully tuning this pathway to ensure effective immune defense without hyperinflammation and immune dysregulation. Here we examine several illustrative cases of IEIs that arise from pathogenic mutations encoding NF-κB inducers, regulators, and NF-κB family components themselves, illuminating how these genes ensure normal adaptive immune system function by maintaining a "Goldilocks effect" state in NF-κB pathway activity.
    MeSH term(s) NF-kappa B/metabolism ; Signal Transduction ; Autoimmunity ; Immune System/metabolism ; Lymphocytes/metabolism
    Chemical Substances NF-kappa B
    Language English
    Publishing date 2023-02-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218531-3
    ISSN 1365-2249 ; 0009-9104 ; 0964-2536
    ISSN (online) 1365-2249
    ISSN 0009-9104 ; 0964-2536
    DOI 10.1093/cei/uxad006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Autosomal Recessive Inflammatory Skin Disease Caused by a Novel Biallelic Loss-of-Function Variant in CARD11.

    Nguyen, Amie / Lu, Henry Y / Turvey, Stuart E / Snow, Andrew L

    Journal of clinical immunology

    2023  Volume 43, Issue 4, Page(s) 709–713

    MeSH term(s) Humans ; Mutation/genetics ; Guanylate Cyclase/genetics ; Dermatitis ; CARD Signaling Adaptor Proteins/genetics
    Chemical Substances Guanylate Cyclase (EC 4.6.1.2) ; CARD11 protein, human (EC 4.6.1.2) ; CARD Signaling Adaptor Proteins
    Language English
    Publishing date 2023-02-02
    Publishing country Netherlands
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 779361-3
    ISSN 1573-2592 ; 0271-9142
    ISSN (online) 1573-2592
    ISSN 0271-9142
    DOI 10.1007/s10875-023-01440-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Elevated IgE from attenuated CARD11 signaling: lessons from atopic mice and humans.

    Pomerantz, Joel L / Milner, Joshua D / Snow, Andrew L

    Current opinion in immunology

    2022  Volume 79, Page(s) 102255

    Abstract: CARD11 encodes a large scaffold protein responsible for integrating antigen-receptor engagement with downstream signaling to NF-kB and other outputs in lymphocytes. Over the past 10 years, several human-inborn errors of immunity have been linked to ... ...

    Abstract CARD11 encodes a large scaffold protein responsible for integrating antigen-receptor engagement with downstream signaling to NF-kB and other outputs in lymphocytes. Over the past 10 years, several human-inborn errors of immunity have been linked to pathogenic CARD11 mutations. Most recently, severe atopic patients were discovered that carried heterozygous dominant-negative CARD11 mutations. Here, we review the mechanistic connections between attenuated CARD11 signaling, elevated IgE, and atopy, comparing and contrasting key insights from both human patients and murine models. Continued investigation of abnormal CARD11 signaling in both contexts should inform novel therapeutic strategies to combat allergic pathogenesis.
    MeSH term(s) Humans ; Mice ; Animals ; CARD Signaling Adaptor Proteins ; Guanylate Cyclase/genetics ; Guanylate Cyclase/metabolism ; Signal Transduction/genetics ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Receptors, Antigen/metabolism
    Chemical Substances CARD Signaling Adaptor Proteins ; Guanylate Cyclase (EC 4.6.1.2) ; NF-kappa B ; Receptors, Antigen ; CARD11 protein, human (EC 4.6.1.2) ; Card11 protein, mouse
    Language English
    Publishing date 2022-11-02
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2022.102255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Molecular and temporal control of restimulation-induced cell death (RICD) in T lymphocytes.

    Lee, Katherine P / Epstein, Benjamin / Lake, Camille M / Snow, Andrew L

    Frontiers in cell death

    2023  Volume 2

    Abstract: For effective adaptive immunity, T lymphocytes must rapidly expand and contract in an antigen-specific manner to effectively control invading pathogens and preserve immunological memory, without sustaining excessive collateral damage to host tissues. ... ...

    Abstract For effective adaptive immunity, T lymphocytes must rapidly expand and contract in an antigen-specific manner to effectively control invading pathogens and preserve immunological memory, without sustaining excessive collateral damage to host tissues. Starting from initial antigen encounter, carefully calibrated programmed cell death pathways are critical for maintaining homeostasis over distinct phases of the T cell response. Restimulation-induced cell death (RICD), a self-regulatory apoptosis pathway triggered by re-engagement of the T cell receptor (TCR), is particularly important for constraining effector T cell expansion to preclude overt immunopathology; indeed, genetic disorders affecting key molecules involved in RICD execution can manifest in excessive lymphoproliferation, malignancy, and autoimmunity. Herein we review our current knowledge of how RICD sensitivity is ultimately regulated over the course of an immune response, including recent revelations on molecules that tune RICD by enforcing resistance or promoting susceptibility in expanding versus mature effector T cells, respectively. Detailed dissection of the molecular and temporal control of RICD also illuminates novel therapeutic strategies for correcting abnormal T cell responses noted in various immune disorders by ultimately tuning RICD sensitivity.
    Language English
    Publishing date 2023-10-30
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2813-5563
    ISSN (online) 2813-5563
    DOI 10.3389/fceld.2023.1281137
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Editorial: CARMA Proteins: Playing a Hand of Four CARDs.

    Bornancin, Frédéric / Snow, Andrew L

    Frontiers in immunology

    2019  Volume 10, Page(s) 1217

    MeSH term(s) Animals ; CARD Signaling Adaptor Proteins/chemistry ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/metabolism ; Humans
    Chemical Substances CARD Signaling Adaptor Proteins
    Language English
    Publishing date 2019-05-29
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2019.01217
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Restimulation-Induced Cell Death (RICD): Methods for Modeling, Investigating, and Quantifying RICD Sensitivity in Primary Human T Cells via Flow Cytometric Analysis.

    Pohida, Katherine / Lake, Camille M / Yee, Debra / Snow, Andrew L

    Bio-protocol

    2022  Volume 12, Issue 4, Page(s) e4326

    Abstract: When the body mounts an immune response against a foreign pathogen, the adaptive arm of the immune system relies upon clonal expansion of antigen-specific T cell populations to exercise acquired effector and cytotoxic functions to clear it. However, T ... ...

    Abstract When the body mounts an immune response against a foreign pathogen, the adaptive arm of the immune system relies upon clonal expansion of antigen-specific T cell populations to exercise acquired effector and cytotoxic functions to clear it. However, T cell expansion must be modulated to effectively combat the perceived threat without inducing excessive collateral damage to host tissues. Restimulation-induced cell death (RICD) is an apoptotic program triggered in activated T cells when an abundance of antigen and IL-2 are present, imposing a negative feedback mechanism that constrains the growing T cell population. This autoregulatory process can be detected via increases in caspase activation, Annexin V binding, and loss of mitochondrial membrane potential. However, simple changes in T cell viability through flow cytometric analysis can reliably measure RICD sensitivity in response to T-cell receptor (TCR) restimulation. This protocol describes the
    Language English
    Publishing date 2022-02-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4326
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: ORMDL3 and Asthma: Linking Sphingolipid Regulation to Altered T Cell Function.

    Luthers, Christopher R / Dunn, Teresa M / Snow, Andrew L

    Frontiers in immunology

    2020  Volume 11, Page(s) 597945

    Abstract: Orosomucoid like 3 (ORMDL3) ...

    Abstract Orosomucoid like 3 (ORMDL3)
    MeSH term(s) Allergens/immunology ; Asthma/etiology ; Asthma/metabolism ; Disease Susceptibility ; Endoplasmic Reticulum Stress ; Energy Metabolism ; Gene Expression Regulation ; Humans ; Immunomodulation ; Lymphocyte Activation/immunology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Sphingolipids/immunology ; Sphingolipids/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
    Chemical Substances Allergens ; Membrane Proteins ; ORMDL3 protein, human ; Sphingolipids
    Language English
    Publishing date 2020-11-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.597945
    Database MEDical Literature Analysis and Retrieval System OnLINE

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