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  1. Artikel ; Online: Dysregulation of Adenosinergic Signaling in Systemic and Organ-Specific Autoimmunity.

    Vuerich, Marta / Harshe, Rasika P / Robson, Simon C / Longhi, Maria Serena

    International journal of molecular sciences

    2019  Band 20, Heft 3

    Abstract: Exact causes for autoimmune diseases remain unclear and no cures are available. Breakdown of immunotolerance could set the stage for unfettered immune responses that target self-antigens. Impaired regulatory immune mechanisms could have permissive roles ... ...

    Abstract Exact causes for autoimmune diseases remain unclear and no cures are available. Breakdown of immunotolerance could set the stage for unfettered immune responses that target self-antigens. Impaired regulatory immune mechanisms could have permissive roles in autoreactivity. Abnormal regulatory immune cell function, therefore, might be a major determinant of the pathogenesis of autoimmune disease. All current treatments are associated with some level of clinical toxicity. Treatment to specifically target dysregulated immunity in these diseases would be a great advance. Extracellular adenosine is a signaling mediator that suppresses inflammation through activation of P1 receptors, most active under pathological conditions. Mounting evidence has linked alterations in the generation of adenosine from extracellular nucleotides by ectonucleotidases, and associated perturbations in purinergic signaling, to the immunological disruption and loss of immunotolerance in autoimmunity. Targeted modulation of the purinergic signaling by either targeting ectonucleotidases or modulating P1 purinergic receptors could therefore restore the balance between autoreactive immune responses; and thereby allow reestablishment of immunotolerance. We review the roles of CD39 and CD73 ectoenzymes in inflammatory states and with the dysregulation of P1 receptor signaling in systemic and organ-specific autoimmunity. Correction of such perturbations could be exploited in potential therapeutic applications.
    Mesh-Begriff(e) Adenosine/metabolism ; Antigens, Neoplasm/metabolism ; Apyrase/metabolism ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/metabolism ; Humans ; Organ Specificity ; Receptors, Purinergic P1/metabolism ; Signal Transduction ; Tetraspanins/metabolism
    Chemische Substanzen Antigens, Neoplasm ; CD37 protein, human ; Receptors, Purinergic P1 ; Tetraspanins ; Apyrase (EC 3.6.1.5) ; ENTPD1 protein, human (EC 3.6.1.5) ; Adenosine (K72T3FS567)
    Sprache Englisch
    Erscheinungsdatum 2019-01-27
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20030528
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Endogenous antisense RNA curbs CD39 expression in Crohn's disease.

    Harshe, Rasika P / Xie, Anyan / Vuerich, Marta / Frank, Luiza Abrahão / Gromova, Barbora / Zhang, Haohai / Robles, Rene' J / Mukherjee, Samiran / Csizmadia, Eva / Kokkotou, Efi / Cheifetz, Adam S / Moss, Alan C / Kota, Satya K / Robson, Simon C / Longhi, Maria Serena

    Nature communications

    2020  Band 11, Heft 1, Seite(n) 5894

    Abstract: CD39 is an ectonucleotidase that initiates conversion of extracellular nucleotides into immunosuppressive adenosine. CD39 is expressed by regulatory T (Treg)-cells, where it mediates immunosuppression, and by a subset of T-helper (Th) 17-cells, where it ... ...

    Abstract CD39 is an ectonucleotidase that initiates conversion of extracellular nucleotides into immunosuppressive adenosine. CD39 is expressed by regulatory T (Treg)-cells, where it mediates immunosuppression, and by a subset of T-helper (Th) 17-cells, where it limits pathogenicity. CD39 is regulated via single-nucleotide-polymorphisms and upon activation of aryl-hydrocarbon-receptor and oxygen-mediated pathways. Here we report a mechanism of CD39 regulation that relies on the presence of an endogenous antisense RNA, transcribed from the 3'-end of the human CD39/ENTPD1 gene. CD39-specific antisense is increased in Treg and Th17-cells of Crohn's disease patients over controls. It largely localizes in the cell nucleus and regulates CD39 by interacting with nucleolin and heterogeneous-nuclear-ribonucleoprotein-A1. Antisense silencing results in CD39 upregulation in vitro and amelioration of disease activity in a trinitro-benzene-sulfonic-acid model of colitis in humanized NOD/scid/gamma mice. Inhibition/blockade of antisense might represent a therapeutic strategy to restore CD39 along with immunohomeostasis in Crohn's disease.
    Mesh-Begriff(e) Animals ; Antigens, CD/genetics ; Antigens, CD/immunology ; Apyrase/genetics ; Apyrase/immunology ; Crohn Disease/genetics ; Crohn Disease/immunology ; Female ; Humans ; Mice ; Mice, Inbred NOD ; RNA, Antisense/genetics ; RNA, Antisense/immunology ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology
    Chemische Substanzen Antigens, CD ; RNA, Antisense ; Apyrase (EC 3.6.1.5) ; CD39 antigen (EC 3.6.1.5)
    Sprache Englisch
    Erscheinungsdatum 2020-11-18
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-19692-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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