{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Han K"],"funding":["Intramural NIH HHS","Medical Research Council","NHLBI NIH HHS","NIH HHS"],"pagination":["101157"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10518596"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(9)"],"pubmed_abstract":["To evaluate whether nicotinamide adenine dinucleotide-positive (NAD<sup>+</sup>) boosting modulates adaptive immunity, primary CD4<sup>+</sup> T cells from healthy control and psoriasis subjects were exposed to vehicle or nicotinamide riboside (NR) supplementation. NR blunts interferon γ (IFNγ) and interleukin (IL)-17 secretion with greater effects on T helper (Th) 17 polarization. RNA sequencing (RNA-seq) analysis implicates NR blunting of sequestosome 1 (sqstm1/p62)-coupled oxidative stress. NR administration increases sqstm1 and reduces reactive oxygen species (ROS) levels. Furthermore, NR activates nuclear factor erythroid 2-related factor 2 (Nrf2), and genetic knockdown of nrf2 and the Nrf2-dependent gene, sqstm1, diminishes NR amelioratory effects. Metabolomics analysis identifies th"],"journal":["Cell reports. Medicine"],"pubmed_title":["Boosting NAD preferentially blunts Th17 inflammation via arginine biosynthesis and redox control in healthy and psoriasis subjects."],"pmcid":["PMC10518596"],"funding_grant_id":["ZIA HL005102","S10 OD021562","MR/P011705/2","R01 HL129510","MR/P011705/1","MR/X012700/1"],"pubmed_authors":["Wu J","Goss-Holmes H","Han K","Sack MN","Sharma R","Griffin JL","Hassanzadeh S","Huffstutler RD","Singh K","Teague HL","Mehta NN","Traba J","Tian R","Meadows AM"],"additional_accession":[]},"is_claimable":false,"name":"Boosting NAD preferentially blunts Th17 inflammation via arginine biosynthesis and redox control in healthy and psoriasis subjects.","description":"To evaluate whether nicotinamide adenine dinucleotide-positive (NAD<sup>+</sup>) boosting modulates adaptive immunity, primary CD4<sup>+</sup> T cells from healthy control and psoriasis subjects were exposed to vehicle or nicotinamide riboside (NR) supplementation. NR blunts interferon γ (IFNγ) and interleukin (IL)-17 secretion with greater effects on T helper (Th) 17 polarization. RNA sequencing (RNA-seq) analysis implicates NR blunting of sequestosome 1 (sqstm1/p62)-coupled oxidative stress. NR administration increases sqstm1 and reduces reactive oxygen species (ROS) levels. Furthermore, NR activates nuclear factor erythroid 2-related factor 2 (Nrf2), and genetic knockdown of nrf2 and the Nrf2-dependent gene, sqstm1, diminishes NR amelioratory effects. Metabolomics analysis identifies th","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Sep","modification":"2026-05-28T12:35:21.124Z","creation":"2025-04-06T18:54:39.107Z"},"accession":"S-EPMC10518596","cross_references":{"pubmed":["37586364"],"doi":["10.1016/j.xcrm.2023.101157"]}}