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  1. Article ; Online: CRACing the role of calcium signaling in ILC2s.

    Falduto, Guido H / Schwartz, Daniella M

    Cell calcium

    2023  Volume 117, Page(s) 102835

    MeSH term(s) Humans ; Immunity, Innate ; Calcium Signaling ; Lymphocytes/metabolism ; Lung/metabolism ; Asthma ; Cytokines/metabolism
    Chemical Substances Cytokines
    Language English
    Publishing date 2023-11-15
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2023.102835
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    Zs.A 1596: Show issues Location:
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  2. Article ; Online: Stepping off the beaten path: A multiomic atlas uncovers novel trajectories of T-cell exhaustion.

    Falduto, Guido H / Schwartz, Daniella M

    Allergy

    2023  Volume 78, Issue 10, Page(s) 2802–2804

    MeSH term(s) Humans ; T-Cell Exhaustion ; Multiomics
    Language English
    Publishing date 2023-05-22
    Publishing country Denmark
    Document type News
    ZDB-ID 391933-x
    ISSN 1398-9995 ; 0105-4538
    ISSN (online) 1398-9995
    ISSN 0105-4538
    DOI 10.1111/all.15770
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  3. Article ; Online: The Complexity of Being A20: From Biological Functions to Genetic Associations.

    Karri, Urekha / Harasimowicz, Magdalena / Carpio Tumba, Manuel / Schwartz, Daniella M

    Journal of clinical immunology

    2024  Volume 44, Issue 3, Page(s) 76

    Abstract: A20, encoded by TNFAIP3, is a critical negative regulator of immune activation. A20 is a ubiquitin editing enzyme with multiple domains, each of which mediates or stabilizes a key ubiquitin modification. A20 targets diverse proteins that are involved in ... ...

    Abstract A20, encoded by TNFAIP3, is a critical negative regulator of immune activation. A20 is a ubiquitin editing enzyme with multiple domains, each of which mediates or stabilizes a key ubiquitin modification. A20 targets diverse proteins that are involved in pleiotropic immunologic pathways. The complexity of A20-mediated immunomodulation is illustrated by the varied effects of A20 deletion in different cell types and disease models. Clinically, the importance of A20 is highlighted by its extensive associations with human disease. A20 germline variants are associated with a wide range of inflammatory diseases, while somatic mutations promote development of B cell lymphomas. More recently, the discovery of A20 haploinsufficiency (HA20) has provided real world evidence for the role of A20 in immune cell function. Originally described as an autosomal dominant form of Behcet's disease, HA20 is now considered a complex inborn error of immunity with a broad spectrum of immunologic and clinical phenotypes.
    MeSH term(s) Humans ; Behcet Syndrome ; Germ-Line Mutation ; Haploinsufficiency ; Immunomodulation ; Ubiquitins ; Tumor Necrosis Factor alpha-Induced Protein 3/chemistry ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics ; Tumor Necrosis Factor alpha-Induced Protein 3/metabolism
    Chemical Substances Ubiquitins ; TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12)
    Language English
    Publishing date 2024-03-07
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 779361-3
    ISSN 1573-2592 ; 0271-9142
    ISSN (online) 1573-2592
    ISSN 0271-9142
    DOI 10.1007/s10875-024-01681-1
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  4. Article ; Online: Hypocrisy of moral imperatives in the Israel-Hamas war.

    Roth, Steven / Wald, Hedy S / Spence, Nicole Z / Oratz, Ruth / Schwartz, Daniella M

    Lancet (London, England)

    2024  Volume 403, Issue 10436, Page(s) 1542

    MeSH term(s) Humans ; Israel ; Morals
    Language English
    Publishing date 2024-04-09
    Publishing country England
    Document type Letter
    ZDB-ID 3306-6
    ISSN 1474-547X ; 0023-7507 ; 0140-6736
    ISSN (online) 1474-547X
    ISSN 0023-7507 ; 0140-6736
    DOI 10.1016/S0140-6736(24)00241-1
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  5. Article ; Online: The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.

    Sylvester, McKella / Son, Aran / Schwartz, Daniella M

    Frontiers in immunology

    2022  Volume 13, Page(s) 818039

    Abstract: Autoinflammatory diseases are a group of clinical syndromes characterized by constitutive overactivation of innate immune pathways. This results in increased production of or responses to monocyte- and neutrophil-derived cytokines such as interleukin-1β ( ...

    Abstract Autoinflammatory diseases are a group of clinical syndromes characterized by constitutive overactivation of innate immune pathways. This results in increased production of or responses to monocyte- and neutrophil-derived cytokines such as interleukin-1β (IL-1β), Tumor Necrosis Factor-α (TNF-α), and Type 1 interferon (IFN). By contrast, clinical allergy is caused by dysregulated type 2 immunity, which is characterized by expansion of T helper 2 (Th2) cells and eosinophils, as well as overproduction of the associated cytokines IL-4, IL-5, IL-9, and IL-13. Traditionally, type 2 immune cells and autoinflammatory effectors were thought to counter-regulate each other. However, an expanding body of evidence suggests that, in some contexts, autoinflammatory pathways and cytokines may potentiate type 2 immune responses. Conversely, type 2 immune cells and cytokines can regulate autoinflammatory responses in complex and context-dependent manners. Here, we introduce the concepts of autoinflammation and type 2 immunity. We proceed to review the mechanisms by which autoinflammatory and type 2 immune responses can modulate each other. Finally, we discuss the epidemiology of type 2 immunity and clinical allergy in several monogenic and complex autoinflammatory diseases. In the future, these interactions between type 2 immunity and autoinflammation may help to expand the spectrum of autoinflammation and to guide the management of patients with various autoinflammatory and allergic diseases.
    MeSH term(s) Cytokines ; Hereditary Autoinflammatory Diseases ; Humans ; Hypersensitivity/complications ; Hypersensitivity/epidemiology ; Interferon Type I ; Tumor Necrosis Factor-alpha
    Chemical Substances Cytokines ; Interferon Type I ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2022-02-24
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.818039
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  6. Article ; Online: Oncogenes calling on a lysosomal Ca

    Schwartz, Daniella M / Muallem, Shmuel

    EMBO reports

    2019  Volume 20, Issue 4

    MeSH term(s) Calcium Signaling ; Lysosomes ; Oncogenes
    Language English
    Publishing date 2019-03-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201947953
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    Zs.A 5433: Show issues Location:
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    Zs.MG 41: Show issues

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  7. Article ; Online: From thymus to tissues and tumors: A review of T-cell biology.

    Chopp, Laura / Redmond, Christopher / O'Shea, John J / Schwartz, Daniella M

    The Journal of allergy and clinical immunology

    2022  Volume 151, Issue 1, Page(s) 81–97

    Abstract: T cells are critical orchestrators of the adaptive immune response that optimally eliminate a specific pathogen. Aberrant T-cell development and function are implicated in a broad range of human disease including immunodeficiencies, autoimmune diseases, ... ...

    Abstract T cells are critical orchestrators of the adaptive immune response that optimally eliminate a specific pathogen. Aberrant T-cell development and function are implicated in a broad range of human disease including immunodeficiencies, autoimmune diseases, and allergic diseases. Accordingly, therapies targeting T cells and their effector cytokines have markedly improved the care of patients with immune dysregulatory diseases. Newer discoveries concerning T-cell-mediated antitumor immunity and T-cell exhaustion have further prompted development of highly effective and novel treatment modalities for malignancies, including checkpoint inhibitors and antigen-reactive T cells. Recent discoveries are also uncovering the depth and variability of T-cell phenotypes: while T cells have long been described using a subset-based classification system, next-generation sequencing technologies suggest an astounding degree of complexity and heterogeneity at the single-cell level.
    MeSH term(s) Humans ; T-Lymphocytes ; Neoplasms ; Adaptive Immunity ; Cytokines ; Immunity, Cellular ; CD8-Positive T-Lymphocytes
    Chemical Substances Cytokines
    Language English
    Publishing date 2022-10-19
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Intramural
    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.2022.10.011
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  8. Article ; Online: Allergic Aspects of IgG4-Related Disease: Implications for Pathogenesis and Therapy.

    Michailidou, Despina / Schwartz, Daniella Muallem / Mustelin, Tomas / Hughes, Grant C

    Frontiers in immunology

    2021  Volume 12, Page(s) 693192

    Abstract: IgG4-related disease (IgG4-RD) is a rare systemic fibroinflammatory disease frequently associated with allergy. The pathogenesis of IgG4-RD is poorly understood, and effective therapies are limited. However, IgG4-RD appears to involve some of the same ... ...

    Abstract IgG4-related disease (IgG4-RD) is a rare systemic fibroinflammatory disease frequently associated with allergy. The pathogenesis of IgG4-RD is poorly understood, and effective therapies are limited. However, IgG4-RD appears to involve some of the same pathogenic mechanisms observed in allergic disease, such as T helper 2 (Th2) and regulatory T cell (Treg) activation, IgG4 and IgE hypersecretion, and blood/tissue eosinophilia. In addition, IgG4-RD tissue fibrosis appears to involve activation of basophils and mast cells and their release of alarmins and cytokines. In this article, we review allergy-like features of IgG4-RD and highlight targeted therapies for allergy that have potential in treating patients with IgG4-RD.
    MeSH term(s) Alarmins/metabolism ; Animals ; Cytokines/metabolism ; Fibrosis ; Humans ; Hypersensitivity/immunology ; Hypersensitivity/metabolism ; Hypersensitivity/physiopathology ; Immune System/immunology ; Immune System/metabolism ; Immune System/physiopathology ; Immunoglobulin E/metabolism ; Immunoglobulin G/immunology ; Immunoglobulin G/metabolism ; Immunoglobulin G4-Related Disease/immunology ; Immunoglobulin G4-Related Disease/metabolism ; Immunoglobulin G4-Related Disease/physiopathology ; Signal Transduction
    Chemical Substances Alarmins ; Cytokines ; Immunoglobulin G ; Immunoglobulin E (37341-29-0)
    Language English
    Publishing date 2021-07-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; 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.2021.693192
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  9. Article ; Online: STIM1 holds a STING in its (N-terminal) tail.

    Son, Aran / de Jesus, Adriana Almeida / Schwartz, Daniella M

    Cell calcium

    2019  Volume 80, Page(s) 192–193

    Abstract: ... The ... ...

    Abstract The Ca
    MeSH term(s) Calcium ; Calcium Channels ; Endoplasmic Reticulum ; Humans ; Interferon Type I ; Membrane Proteins ; Neoplasm Proteins ; Stromal Interaction Molecule 1
    Chemical Substances Calcium Channels ; Interferon Type I ; Membrane Proteins ; Neoplasm Proteins ; STIM1 protein, human ; Stromal Interaction Molecule 1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2019-03-07
    Publishing country Netherlands
    Document type Journal Article ; Comment
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2019.03.003
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  10. Article ; Online: JAK-STAT signaling in human disease: From genetic syndromes to clinical inhibition.

    Luo, Yiming / Alexander, Madison / Gadina, Massimo / O'Shea, John J / Meylan, Francoise / Schwartz, Daniella M

    The Journal of allergy and clinical immunology

    2021  Volume 148, Issue 4, Page(s) 911–925

    Abstract: Since its discovery, the Janus kinase-signal transduction and activation of transcription (JAK-STAT) pathway has become recognized as a central mediator of widespread and varied human physiological processes. The field of JAK-STAT biology, particularly ... ...

    Abstract Since its discovery, the Janus kinase-signal transduction and activation of transcription (JAK-STAT) pathway has become recognized as a central mediator of widespread and varied human physiological processes. The field of JAK-STAT biology, particularly its clinical relevance, continues to be shaped by 2 important advances. First, the increased use of genomic sequencing has led to the discovery of novel clinical syndromes caused by mutations in JAK and STAT genes. This has provided insights regarding the consequences of aberrant JAK-STAT signaling for immunity, lymphoproliferation, and malignancy. In addition, since the approval of ruxolitinib and tofacitinib, the therapeutic use of JAK inhibitors (jakinibs) has expanded to include a large spectrum of diseases. Efficacy and safety data from over a decade of clinical studies have provided additional mechanistic insights while improving the care of patients with inflammatory and neoplastic conditions. This review discusses major advances in the field, focusing on updates in genetic diseases and in studies of clinical jakinibs in human disease.
    MeSH term(s) Animals ; Cytokines/immunology ; Genetic Diseases, Inborn/drug therapy ; Genetic Diseases, Inborn/immunology ; Humans ; Janus Kinase Inhibitors/therapeutic use ; Janus Kinases/genetics ; Janus Kinases/immunology ; Mutation ; STAT Transcription Factors/genetics ; STAT Transcription Factors/immunology ; Signal Transduction
    Chemical Substances Cytokines ; Janus Kinase Inhibitors ; STAT Transcription Factors ; Janus Kinases (EC 2.7.10.2)
    Language English
    Publishing date 2021-10-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    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.2021.08.004
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