ArticleCell2015
CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity.
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Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers.
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238citing papers in PubMed
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238 citing papers in PubMed, 395 citations in OpenAlex.
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- CD5L insufficiency exacerbates skeletal joint damage in rheumatoid arthritis.Molecular medicine (Cambridge, Mass.) · 2026Article
- ODC1 restricts meningeal B cell age-associated-like phenotype and function in multiple sclerosis: A human and experimental study.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026Review
- Proteomics profiling of serum and liver in GSD Ia and Ib patients: insights into complication mechanisms and circulation biomarkers.Journal of translational medicine · 2026Article
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- The pivotal role of immunometabolism in diabetic neuropathy and its potential therapeutic strategies.Frontiers in endocrinology · 2026Review
- Fatty acid metabolism-an emerging regulatory node in T-cell immunometabolism.Clinical & translational immunology · 2026Review
- Pro-Inflammatory c-MetAnnals of neurology · 2026Article
- Tumoral ALOX5 mediated arachidonic acid metabolism regulates immune response in non-small cell lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- IL-18 drives the Bhlhe40-mediated pathogenic Th17 cell response and exacerbates autoimmune disease progression.Cellular & molecular immunology · 2025Article
- Fructose intake driven glycolysis-ROS-EGFR axis specifically promotes the generation and pathogenicity of Th17 cells.Nature communications · 2025Article
- Autoimmune disease risk gene ANKRD55 promotes TH17 effector function through metabolic modulation.The Journal of experimental medicine · 2025Article
- Discovery of core genes for systemic lupus erythematosus via genome-wide aggregated trans-effects analysis.Genes and immunity · 2025Article
178 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 5 institutions in 2 countries.
Chao WangEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Nir YosefBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA; Department of Electrical Engineering and Computer Science, University of California, Berkeley, Berkeley, CA 94720, USA; Center for Computational Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Jellert GaublommeBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA; Department of Chemistry and Chemical Biology and Department of Physics, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA.
Chuan WuEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Youjin LeeEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Clary B ClishBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
Jim KaminskiCenter for Computational Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
Sheng XiaoEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Gerd Meyer Zu HorsteEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Mathias PawlakEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Yasuhiro KishiEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Mitsubishi Tanabe Pharma Corporation, Kamoshida-cho 1000, Yokohama, 225-0002, Japan.
Nicole JollerEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Katarzyna KarwaczEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Chen ZhuEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Maria Ordovas-MontanesEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Asaf MadiEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
Ivo WortmanBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
Toru MiyazakiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.
Raymond A SobelPalo Alto Veteran's Administration Health Care System and Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Hongkun ParkBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA; Department of Chemistry and Chemical Biology and Department of Physics, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA.
Aviv RegevBroad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA; Howard Hughes Medical Institute and David H. Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 20140, USA. Electronic address: aregev@broadinstitute.org.
Vijay K KuchrooEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA. Electronic address: vkuchroo@evergrande.hms.harvard.edu.
Brigham and Women's Hospital · USBroad Institute · USThe University of Tokyo · JPUniversity of California, Berkeley · USVA Palo Alto Health Care System · US
Funding
VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Kristin A Knouse · 1985 to 2026
$93.9MRole of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7MTransgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BLAZAR, BRUCE R · 2003 to 2023
$42.5MTCR recognition of MHC class II peptide compexes in multiple sclerosisP01AI045757 · NIAID · DANA-FARBER CANCER INSTITUTE · PI KUCHROO, VIJAY K., LOVE, JOHN CHRISTOPHER · 1999 to 2017
$22.8MCenter for Cell CircuitsP50HG006193 · NHGRI · BROAD INSTITUTE, INC. · PI REGEV, AVIV · 2011 to 2015
$15.6MTranscriptional regulations of effector and regulatory T cells in EAEP01NS076410 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUCHROO, VIJAY K. · 2013 to 2017
$5.6MT CELL RESPONSE TO MYELIN PROTEOLIPID PROTEINR01NS030843 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUCHROO, VIJAY K. · 1998 to 2019
$4.1MT cell response to myelin proteolipid proteinR37NS030843 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI KUCHROO, VIJAY K. · 2002 to 2008
$2.6MMolecular signatures of high salt induced pathogenic T cellsR00AI110649 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WU, CHUAN · 2015 to 2016
$498kTCELL RESPONSE TO MYELIN PROTEOLIPID PROTEINR29NS030843 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KUCHROO, VIJAY K · 1992 to 1996
–Howard Hughes Medical InstituteNCI NIH HHS P30 CA014051NHGRI NIH HHS P50 HG006193NIAID NIH HHS 4R00AI110649NIAID NIH HHS AI039671NIAID NIH HHS AI056299NIAID NIH HHS P01 AI039671NIAID NIH HHS P01 AI045757NIAID NIH HHS P01 AI056299NIAID NIH HHS R00 AI110649NINDS NIH HHS NS030843NINDS NIH HHS NS076410NINDS NIH HHS P01 NS076410NINDS NIH HHS R01 NS030843NINDS NIH HHS R29 NS030843NINDS NIH HHS R37 NS030843
Abstract
Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing "pathogenic" and "non-pathogenic" Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a regulator expressed in non-pathogenic, but not in pathogenic Th17 cells. Although CD5L does not affect Th17 differentiation, it is a functional switch that regulates the pathogenicity of Th17 cells. Loss of CD5L converts non-pathogenic Th17 cells into pathogenic cells that induce autoimmunity. CD5L mediates this effect by modulating the intracellular lipidome, altering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability for Rorγt, the master transcription factor of Th17 cells. Our study identifies CD5L as a critical regulator of the Th17 cell functional state and highlights the importance of lipid metabolism in balancing immune protection and disease induced by T cells.
Indexed as
Lipid MetabolismAnimalsApoptosis Regulatory ProteinsCell DifferentiationCentral Nervous SystemCholesterolEncephalomyelitis, Autoimmune, ExperimentalFatty Acids, UnsaturatedHumansLymph NodesMiceNuclear Receptor Subfamily 1, Group F, Member 3Receptors, ImmunologicReceptors, ScavengerReceptor Tyrosine Kinase-like Orphan ReceptorsSingle-Cell AnalysisApoptosis Regulatory ProteinsCd5l protein, mouseCholesterolFatty Acids, UnsaturatedNuclear Receptor Subfamily 1, Group F, Member 3Receptors, ImmunologicReceptors, ScavengerReceptor Tyrosine Kinase-like Orphan ReceptorsRorc protein, mouse
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