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  1. Article ; Online: Do multiple subsets of CD11c

    Tangye, Stuart G

    The Journal of allergy and clinical immunology

    2023  Volume 152, Issue 3, Page(s) 607–609

    MeSH term(s) Humans ; B-Lymphocytes ; B-Lymphocyte Subsets ; CD11c Antigen
    Chemical Substances CD11c Antigen
    Language English
    Publishing date 2023-07-24
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2023.07.004
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  2. Article ; Online: For whom the B(c)ell tolls: CXCL4 AIDs human autoimmunity.

    Tangye, Stuart G

    The Journal of experimental medicine

    2023  Volume 220, Issue 12

    Abstract: In this issue of JEM, Çakan et al. (2023. J. Exp. Med.https://doi.org/10.1084/jem.20230944) explore a CXCL4-mediated mechanism by which TLRs cause autoimmunity in human B cells, breaching bone marrow tolerance. ...

    Abstract In this issue of JEM, Çakan et al. (2023. J. Exp. Med.https://doi.org/10.1084/jem.20230944) explore a CXCL4-mediated mechanism by which TLRs cause autoimmunity in human B cells, breaching bone marrow tolerance.
    MeSH term(s) Humans ; Autoimmunity ; Bone Marrow
    Language English
    Publishing date 2023-09-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20231397
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  3. Article ; Online: Impact of SARS-CoV-2 infection and COVID-19 on patients with inborn errors of immunity.

    Tangye, Stuart G

    The Journal of allergy and clinical immunology

    2022  Volume 151, Issue 4, Page(s) 818–831

    Abstract: Since the arrival of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, its characterization as a novel human pathogen, and the resulting coronavirus disease 2019 (COVID-19) pandemic, over 6.5 million people have died ... ...

    Abstract Since the arrival of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, its characterization as a novel human pathogen, and the resulting coronavirus disease 2019 (COVID-19) pandemic, over 6.5 million people have died worldwide-a stark and sobering reminder of the fundamental and nonredundant roles of the innate and adaptive immune systems in host defense against emerging pathogens. Inborn errors of immunity (IEI) are caused by germline variants, typically in single genes. IEI are characterized by defects in development and/or function of cells involved in immunity and host defense, rendering individuals highly susceptible to severe, recurrent, and sometimes fatal infections, as well as immune dysregulatory conditions such as autoinflammation, autoimmunity, and allergy. The study of IEI has revealed key insights into the molecular and cellular requirements for immune-mediated protection against infectious diseases. Indeed, this has been exemplified by assessing the impact of SARS-CoV-2 infection in individuals with previously diagnosed IEI, as well as analyzing rare cases of severe COVID-19 in otherwise healthy individuals. This approach has defined fundamental aspects of mechanisms of disease pathogenesis, immunopathology in the context of infection with a novel pathogen, and therapeutic options to mitigate severe disease. This review summarizes these findings and illustrates how the study of these rare experiments of nature can inform key features of human immunology, which can then be leveraged to improve therapies for treating emerging and established infectious diseases.
    MeSH term(s) Humans ; COVID-19 ; SARS-CoV-2 ; Disease Susceptibility ; Communicable Diseases
    Language English
    Publishing date 2022-12-13
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2022.11.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The Th17/IL-17 Axis and Host Defense Against Fungal Infections.

    Tangye, Stuart G / Puel, Anne

    The journal of allergy and clinical immunology. In practice

    2023  Volume 11, Issue 6, Page(s) 1624–1634

    Abstract: Chronic mucocutaneous candidiasis (CMC) was recognized as a primary immunodeficiency in the early 1970s. However, for almost 40 years, its genetic etiology remained unknown. The progressive molecular and cellular description of inborn errors of immunity ( ...

    Abstract Chronic mucocutaneous candidiasis (CMC) was recognized as a primary immunodeficiency in the early 1970s. However, for almost 40 years, its genetic etiology remained unknown. The progressive molecular and cellular description of inborn errors of immunity (IEI) with syndromic CMC pointed toward a possible role of IL-17-mediated immunity in protecting against fungal infection and CMC. Since 2011, novel IEI affecting either the response to or production of IL-17A and/or IL-17F (IL-17A/F) in patients with isolated or syndromic CMC provided formal proof of the pivotal role of the IL-17 axis in mucocutaneous immunity to Candida spp, and, to a lesser extent, to Staphylococcus aureus in humans. In contrast, IL-17-mediated immunity seems largely redundant against other common microbes in humans. In this review, we outline the current knowledge of IEI associated with impaired IL-17A/F-mediated immunity, highlighting our current understanding of the role of IL-17A/F in human immunity.
    MeSH term(s) Humans ; Interleukin-17 ; Candidiasis, Chronic Mucocutaneous/genetics ; Th17 Cells ; Staphylococcal Infections
    Chemical Substances Interleukin-17
    Language English
    Publishing date 2023-04-26
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2843237-X
    ISSN 2213-2201 ; 2213-2198
    ISSN (online) 2213-2201
    ISSN 2213-2198
    DOI 10.1016/j.jaip.2023.04.015
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  5. Article ; Online: DOCK11

    Tangye, Stuart G / Meyts, Isabelle

    The New England journal of medicine

    2023  Volume 389, Issue 6, Page(s) 563–567

    MeSH term(s) Humans ; Immune System Diseases/complications ; Immune System Diseases/genetics ; Guanine Nucleotide Exchange Factors/genetics
    Chemical Substances Guanine Nucleotide Exchange Factors
    Language English
    Publishing date 2023-08-17
    Publishing country United States
    Document type Editorial
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe2305431
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  6. Article ; Online: Inborn errors of immunity: the Goldilocks effect-susceptibility to disease due to a little too much or a little too little.

    Ma, Cindy S / Tangye, Stuart G

    Clinical and experimental immunology

    2023  Volume 212, Issue 2, Page(s) 93–95

    Language English
    Publishing date 2023-04-12
    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/uxad039
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  7. Article ; Online: Genetic susceptibility to EBV infection: insights from inborn errors of immunity.

    Tangye, Stuart G

    Human genetics

    2020  Volume 139, Issue 6-7, Page(s) 885–901

    Abstract: Epstein-Barr virus (EBV) is a ubiquitous human pathogen, infecting > 90% of the adult population. In the vast majority of healthy individuals, infection with EBV runs a relatively benign course. However, EBV is by no means a benign pathogen. Indeed, ... ...

    Abstract Epstein-Barr virus (EBV) is a ubiquitous human pathogen, infecting > 90% of the adult population. In the vast majority of healthy individuals, infection with EBV runs a relatively benign course. However, EBV is by no means a benign pathogen. Indeed, apart from being associated with at least seven different types of malignancies, EBV infection can cause severe and often fatal diseases-hemophagocytic lymphohistiocytosis, lymphoproliferative disease, B-cell lymphoma-in rare individuals with specific monogenic inborn errors of immunity. The discovery and detailed investigation of inborn errors of immunity characterized by heightened susceptibility to, or increased frequency of, EBV-induced disease have elegantly revealed cell types and signaling pathways that play critical and non-redundant roles in host-defense against EBV. These analyses have revealed not only mechanisms underlying EBV-induced disease in rare genetic conditions, but also identified molecules and pathways that could be targeted to treat severe EBV infection and pathological consequences in immunodeficient hosts, or even potentially enhance the efficacy of an EBV-specific vaccine.
    MeSH term(s) Epstein-Barr Virus Infections/complications ; Epstein-Barr Virus Infections/immunology ; Epstein-Barr Virus Infections/virology ; Genetic Predisposition to Disease ; Herpesvirus 4, Human/genetics ; Herpesvirus 4, Human/immunology ; Host-Pathogen Interactions/genetics ; Humans ; Immunologic Deficiency Syndromes/complications ; Immunologic Deficiency Syndromes/immunology ; Immunologic Deficiency Syndromes/virology ; Lymphoproliferative Disorders/etiology ; Lymphoproliferative Disorders/pathology ; Signal Transduction
    Language English
    Publishing date 2020-03-09
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 223009-4
    ISSN 1432-1203 ; 0340-6717
    ISSN (online) 1432-1203
    ISSN 0340-6717
    DOI 10.1007/s00439-020-02145-3
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  8. Article ; Online: It's that time of year-APRIL promotes humoral immunity in humans.

    Tangye, Stuart G

    The Journal of allergy and clinical immunology

    2020  Volume 146, Issue 5, Page(s) 1013–1015

    MeSH term(s) Humans ; Immunity, Humoral ; Immunoglobulins ; Plasma Cells ; Tumor Necrosis Factor Ligand Superfamily Member 13
    Chemical Substances Immunoglobulins ; TNFSF13 protein, human ; Tumor Necrosis Factor Ligand Superfamily Member 13
    Language English
    Publishing date 2020-09-21
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2020.09.005
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  9. Article ; Online: "Are you gonna go my way?"-Decisions at the Tfh-B cell interface.

    Tangye, Stuart G / Warnatz, Klaus

    Immunity

    2022  Volume 55, Issue 3, Page(s) 377–379

    Abstract: The generation of memory B cells and plasma cells is complex and involves inputs from the microenvironment, notably from T follicular helper cells. In last month's issue of Immunity, Yeh et al. and Song et al. refine our understanding of the B cell ... ...

    Abstract The generation of memory B cells and plasma cells is complex and involves inputs from the microenvironment, notably from T follicular helper cells. In last month's issue of Immunity, Yeh et al. and Song et al. refine our understanding of the B cell intrinsic and extrinsic requirements to generate effective humoral immunity in response to foreign antigens.
    MeSH term(s) B-Lymphocytes/immunology ; Germinal Center/immunology ; Immunity, Humoral/immunology ; Programmed Cell Death 1 Receptor ; Receptors, CXCR5 ; T Follicular Helper Cells ; T-Lymphocytes, Helper-Inducer/immunology
    Chemical Substances Programmed Cell Death 1 Receptor ; Receptors, CXCR5
    Language English
    Publishing date 2022-02-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2022.02.002
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  10. Article ; Online: Cytokine-mediated STAT-dependent pathways underpinning human B-cell differentiation and function.

    Tangye, Stuart G / Pathmanandavel, Karrnan / Ma, Cindy S

    Current opinion in immunology

    2023  Volume 81, Page(s) 102286

    Abstract: B cells are fundamental to host defence against infectious diseases; indeed, the ability of humans to elicit robust antibody responses following exposure to foreign antigens underpins long-lived humoral immunity and serological memory, as well as the ... ...

    Abstract B cells are fundamental to host defence against infectious diseases; indeed, the ability of humans to elicit robust antibody responses following exposure to foreign antigens underpins long-lived humoral immunity and serological memory, as well as the success of most currently administered vaccines. However, B cells also have a dark side - they can cause myriad diseases, including autoimmunity, atopy, allergy and malignancy. Thus, it is critical to understand the molecular requirements for generating effective, high-affinity, specific immune responses following natural infection or vaccination, as well as for constraining B-cell function to mitigate B-cell-mediated immune dyscrasias. In this review, we discuss recent developments that have been derived from the identification and detailed analysis of individuals with inborn errors of immunity that disrupt cytokine signalling, resulting in immune dysregulatory conditions. These studies have defined fundamental cytokine/cytokine receptor/signal transducer and activator of transcription (STAT) signalling pathways that are critical for the generation and maintenance of human memory B-cell and plasma cell subsets during host defence, as well as revealed mechanisms of disease pathogenesis causing immune deficiency, autoimmunity and atopy. More importantly, these studies have identified molecules that could be targeted to either enhance humoral immunity in the settings of infection or vaccination, or attenuate humoral immunity that contributes to antibody-mediated autoimmunity or allergy.
    MeSH term(s) Humans ; Cytokines ; B-Lymphocytes ; Immunity, Humoral ; Cell Differentiation ; Hypersensitivity
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-02-08
    Publishing country England
    Document type Journal Article ; Review ; 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.2023.102286
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