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  1. Article ; Online: Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes

    Jinxiu Rui / Songyan Deng / Ana Luisa Perdigoto / Gerald Ponath / Romy Kursawe / Nathan Lawlor / Tomokazu Sumida / Maya Levine-Ritterman / Michael L. Stitzel / David Pitt / Jun Lu / Kevan C. Herold

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Volume 13

    Abstract: There are dynamic interactions between immune cells and β cells that lead to β cell destruction in the context of autoimmune diabetes. Here the authors show that TET2, a methylcytosine dioxygenase, can regulate this interaction and deletion of TET2 can ... ...

    Abstract There are dynamic interactions between immune cells and β cells that lead to β cell destruction in the context of autoimmune diabetes. Here the authors show that TET2, a methylcytosine dioxygenase, can regulate this interaction and deletion of TET2 can prevent the autoimmune destruction of β cells in mice.
    Keywords Science ; Q
    Language English
    Publishing date 2021-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Immune cells and their inflammatory mediators modify β cells and cause checkpoint inhibitor–induced diabetes

    Ana Luisa Perdigoto / Songyan Deng / Katherine C. Du / Manik Kuchroo / Daniel B. Burkhardt / Alexander Tong / Gary Israel / Marie E. Robert / Stuart P. Weisberg / Nancy Kirkiles-Smith / Angeliki M. Stamatouli / Harriet M. Kluger / Zoe Quandt / Arabella Young / Mei-Ling Yang / Mark J. Mamula / Jordan S. Pober / Mark S. Anderson / Smita Krishnaswamy /
    Kevan C. Herold

    JCI Insight, Vol 7, Iss

    2022  Volume 17

    Abstract: Checkpoint inhibitors (CPIs) targeting programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) have revolutionized cancer treatment but can trigger autoimmune complications, including CPI-induced diabetes ...

    Abstract Checkpoint inhibitors (CPIs) targeting programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) have revolutionized cancer treatment but can trigger autoimmune complications, including CPI-induced diabetes mellitus (CPI-DM), which occurs preferentially with PD-1 blockade. We found evidence of pancreatic inflammation in patients with CPI-DM with shrinkage of pancreases, increased pancreatic enzymes, and in a case from a patient who died with CPI-DM, peri-islet lymphocytic infiltration. In the NOD mouse model, anti–PD-L1 but not anti–CTLA-4 induced diabetes rapidly. RNA sequencing revealed that cytolytic IFN-γ+CD8+ T cells infiltrated islets with anti–PD-L1. Changes in β cells were predominantly driven by IFN-γ and TNF-α and included induction of a potentially novel β cell population with transcriptional changes suggesting dedifferentiation. IFN-γ increased checkpoint ligand expression and activated apoptosis pathways in human β cells in vitro. Treatment with anti–IFN-γ and anti–TNF-α prevented CPI-DM in anti–PD-L1–treated NOD mice. CPIs targeting the PD-1/PD-L1 pathway resulted in transcriptional changes in β cells and immune infiltrates that may lead to the development of diabetes. Inhibition of inflammatory cytokines can prevent CPI-DM, suggesting a strategy for clinical application to prevent this complication.
    Keywords Autoimmunity ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-09-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    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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