<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Jadon N</submitter><funding>U.S. Department of Defense</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>Induced regulatory T cells (iTregs) are a heterogeneous population of immunosuppressive T cells with therapeutic potential. Treg cells show a range of plasticity and can acquire T effector-like capacities, as is the case for T helper 1 (Th1)-like iTregs. Thus, it is important to distinguish between functional plasticity and lineage instability. Aplastic anemia (AA) is an autoimmune disorder characterized by immune-mediated destruction of hematopoietic stem and progenitor cells in the bone marrow (BM). Th1-like 1 iTregs can be potent suppressors of aberrant Th1-mediated immune responses such as those that drive AA disease progression. Here we investigated the function of the epigenetic enzyme, protein arginine methyltransferase 5 (PRMT5), its regulation of the iTreg-desta</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1292049</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10800960</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PRMT5 regulates epigenetic changes in suppressive Th1-like iTregs in response to IL-12 treatment.</pubmed_title><pmcid>PMC10800960</pmcid><pubmed_authors>Jadon N</pubmed_authors><pubmed_authors>Minter LM</pubmed_authors><pubmed_authors>Shanthalingam S</pubmed_authors><pubmed_authors>Tew GN</pubmed_authors></additional><is_claimable>false</is_claimable><name>PRMT5 regulates epigenetic changes in suppressive Th1-like iTregs in response to IL-12 treatment.</name><description>&lt;h4>Background&lt;/h4>Induced regulatory T cells (iTregs) are a heterogeneous population of immunosuppressive T cells with therapeutic potential. Treg cells show a range of plasticity and can acquire T effector-like capacities, as is the case for T helper 1 (Th1)-like iTregs. Thus, it is important to distinguish between functional plasticity and lineage instability. Aplastic anemia (AA) is an autoimmune disorder characterized by immune-mediated destruction of hematopoietic stem and progenitor cells in the bone marrow (BM). Th1-like 1 iTregs can be potent suppressors of aberrant Th1-mediated immune responses such as those that drive AA disease progression. Here we investigated the function of the epigenetic enzyme, protein arginine methyltransferase 5 (PRMT5), its regulation of the iTreg-desta</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2026-07-15T10:03:59.133Z</modification><creation>2024-11-20T13:19:58.984Z</creation></dates><accession>S-EPMC10800960</accession><cross_references><pubmed>38259494</pubmed><doi>10.3389/fimmu.2023.1292049</doi></cross_references></HashMap>