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  1. Article ; Online: Loss of TET2 and TET3 in regulatory T cells unleashes effector function

    Xiaojing Yue / Chan-Wang J. Lio / Daniela Samaniego-Castruita / Xiang Li / Anjana Rao

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 14

    Abstract: Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells ... ...

    Abstract Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells and bystander T cells gain aberrant effector function.
    Keywords Science ; Q
    Language English
    Publishing date 2019-05-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  2. Article ; Online: Loss of TET2 and TET3 in regulatory T cells unleashes effector function

    Xiaojing Yue / Chan-Wang J. Lio / Daniela Samaniego-Castruita / Xiang Li / Anjana Rao

    Nature Communications, Vol 10, Iss 1, Pp 1-

    2019  Volume 14

    Abstract: Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells ... ...

    Abstract Loss of TET proteins in immune cell populations is known to result in immunopathology. Here the authors show that deficiency of Tet2 and Tet3 proteins, specifically in the CD4+ FoxP3+ Treg lineage, results in a dominant pathology in which ex-Treg cells and bystander T cells gain aberrant effector function.
    Keywords Science ; Q
    Language English
    Publishing date 2019-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  3. Article ; Online: Aiolos represses CD4+ T cell cytotoxic programming via reciprocal regulation of TFH transcription factors and IL-2 sensitivity

    Kaitlin A. Read / Devin M. Jones / Srijana Pokhrel / Emily D. S. Hales / Aditi Varkey / Jasmine A. Tuazon / Caprice D. Eisele / Omar Abdouni / Abbey Saadey / Melissa R. Leonard / Robert T. Warren / Michael D. Powell / Jeremy M. Boss / Emily A. Hemann / Jacob S. Yount / Gang Xin / Hazem E. Ghoneim / Chan-Wang J. Lio / Aharon G. Freud /
    Patrick L. Collins / Kenneth J. Oestreich

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 18

    Abstract: The regulation and direction of CD4+ T cells into phenotypic and functional lineages is coordinated by a complex set of mechanisms. Here the authors show a role for Aiolos as a regulator of the CD4+ cytotoxic and T follicular helper lineages. ...

    Abstract The regulation and direction of CD4+ T cells into phenotypic and functional lineages is coordinated by a complex set of mechanisms. Here the authors show a role for Aiolos as a regulator of the CD4+ cytotoxic and T follicular helper lineages.
    Keywords Science ; Q
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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