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  1. Artikel ; Online: Elevated transferrin receptor impairs T cell metabolism and function in systemic lupus erythematosus.

    Voss, Kelsey / Sewell, Allison E / Krystofiak, Evan S / Gibson-Corley, Katherine N / Young, Arissa C / Basham, Jacob H / Sugiura, Ayaka / Arner, Emily N / Beavers, William N / Kunkle, Dillon E / Dickson, Megan E / Needle, Gabriel A / Skaar, Eric P / Rathmell, W Kimryn / Ormseth, Michelle J / Major, Amy S / Rathmell, Jeffrey C

    Science immunology

    2023  Band 8, Heft 79, Seite(n) eabq0178

    Abstract: T cells in systemic lupus erythematosus (SLE) exhibit multiple metabolic abnormalities. Excess iron can impair mitochondria and may contribute to SLE. To gain insights into this potential role of iron in SLE, we performed a CRISPR screen of iron handling ...

    Abstract T cells in systemic lupus erythematosus (SLE) exhibit multiple metabolic abnormalities. Excess iron can impair mitochondria and may contribute to SLE. To gain insights into this potential role of iron in SLE, we performed a CRISPR screen of iron handling genes on T cells. Transferrin receptor (CD71) was identified as differentially critical for T
    Mesh-Begriff(e) Animals ; Mice ; Interleukin-10/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Receptors, Transferrin/metabolism ; T-Lymphocytes, Regulatory/metabolism ; Humans
    Chemische Substanzen Interleukin-10 (130068-27-8) ; Receptors, Transferrin
    Sprache Englisch
    Erscheinungsdatum 2023-01-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abq0178
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: MTHFD2 is a metabolic checkpoint controlling effector and regulatory T cell fate and function.

    Sugiura, Ayaka / Andrejeva, Gabriela / Voss, Kelsey / Heintzman, Darren R / Xu, Xincheng / Madden, Matthew Z / Ye, Xiang / Beier, Katherine L / Chowdhury, Nowrin U / Wolf, Melissa M / Young, Arissa C / Greenwood, Dalton L / Sewell, Allison E / Shahi, Shailesh K / Freedman, Samantha N / Cameron, Alanna M / Foerch, Patrik / Bourne, Tim / Garcia-Canaveras, Juan C /
    Karijolich, John / Newcomb, Dawn C / Mangalam, Ashutosh K / Rabinowitz, Joshua D / Rathmell, Jeffrey C

    Immunity

    2021  Band 55, Heft 1, Seite(n) 65–81.e9

    Abstract: Antigenic stimulation promotes T cell metabolic reprogramming to meet increased biosynthetic, bioenergetic, and signaling demands. We show that the one-carbon (1C) metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) regulates de novo ... ...

    Abstract Antigenic stimulation promotes T cell metabolic reprogramming to meet increased biosynthetic, bioenergetic, and signaling demands. We show that the one-carbon (1C) metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) regulates de novo purine synthesis and signaling in activated T cells to promote proliferation and inflammatory cytokine production. In pathogenic T helper-17 (Th17) cells, MTHFD2 prevented aberrant upregulation of the transcription factor FoxP3 along with inappropriate gain of suppressive capacity. MTHFD2 deficiency also promoted regulatory T (Treg) cell differentiation. Mechanistically, MTHFD2 inhibition led to depletion of purine pools, accumulation of purine biosynthetic intermediates, and decreased nutrient sensor mTORC1 signaling. MTHFD2 was also critical to regulate DNA and histone methylation in Th17 cells. Importantly, MTHFD2 deficiency reduced disease severity in multiple in vivo inflammatory disease models. MTHFD2 is thus a metabolic checkpoint to integrate purine metabolism with pathogenic effector cell signaling and is a potential therapeutic target within 1C metabolism pathways.
    Mesh-Begriff(e) Animals ; Cell Differentiation ; Cytokines/metabolism ; DNA Methylation ; Disease Models, Animal ; Humans ; Inflammation/immunology ; Inflammation Mediators/metabolism ; Lymphocyte Activation ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Methylenetetrahydrofolate Dehydrogenase (NADP)/genetics ; Methylenetetrahydrofolate Dehydrogenase (NADP)/metabolism ; Mice ; Mice, Transgenic ; Mutation/genetics ; Purines/biosynthesis ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology
    Chemische Substanzen Cytokines ; Inflammation Mediators ; Purines ; Methylenetetrahydrofolate Dehydrogenase (NADP) (EC 1.5.1.5) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2021-11-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.10.011
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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