KIR <sup>+</sup> CD8 <sup>+</sup> T cells suppress pathogenic T cells and are active in autoimmune diseases and COVID-19

DOI Web Site 被引用文献4件
  • Jing Li
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Maxim Zaslavsky
    Program in Computer Science, Stanford University, Stanford, CA, USA.
  • Yapeng Su
    Institute for Systems Biology, Seattle, WA, USA.
  • Jing Guo
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.
  • Michael J. Sikora
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Vincent van Unen
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Asbjørn Christophersen
    K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
  • Shin-Heng Chiou
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Liang Chen
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Jiefu Li
    The Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA.
  • Xuhuai Ji
    Human Immune Monitoring Center, Stanford University School of Medicine, Stanford, CA, USA.
  • Julie Wilhelmy
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Alana M. McSween
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Brad A. Palanski
    Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Venkata Vamsee Aditya Mallajosyula
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Nathan A. Bracey
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Gopal Krishna R. Dhondalay
    Sean N. Parker Center for Allergy and Asthma Research, Department of Medicine, Stanford University, Stanford, CA, USA.
  • Kartik Bhamidipati
    Program in Immunology, Stanford University School of Medicine, Stanford, CA, USA.
  • Joy Pai
    Program in Immunology, Stanford University School of Medicine, Stanford, CA, USA.
  • Lucas B. Kipp
    Division of Neuroimmunology, Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
  • Jeffrey E. Dunn
    Division of Neuroimmunology, Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
  • Stephen L. Hauser
    Department of Neurology and UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA.
  • Jorge R. Oksenberg
    Department of Neurology and UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA.
  • Ansuman T. Satpathy
    Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
  • William H. Robinson
    VA Palo Alto Health Care System, Palo Alto, CA, USA.
  • Cornelia L. Dekker
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.
  • Lars M. Steinmetz
    Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • Chaitan Khosla
    Department of Chemistry, Stanford University, Stanford, CA, USA.
  • Paul J. Utz
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Ludvig M. Sollid
    K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
  • Yueh-Hsiu Chien
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • James R. Heath
    Institute for Systems Biology, Seattle, WA, USA.
  • Nielsen Q. Fernandez-Becker
    Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University, Stanford, CA, USA.
  • Kari C. Nadeau
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Naresha Saligrama
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • Mark M. Davis
    Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.

抄録

<jats:p> In this work, we find that CD8 <jats:sup>+</jats:sup> T cells expressing inhibitory killer cell immunoglobulin-like receptors (KIRs) are the human equivalent of Ly49 <jats:sup>+</jats:sup> CD8 <jats:sup>+</jats:sup> regulatory T cells in mice and are increased in the blood and inflamed tissues of patients with a variety of autoimmune diseases. Moreover, these CD8 <jats:sup>+</jats:sup> T cells efficiently eliminated pathogenic gliadin-specific CD4 <jats:sup>+</jats:sup> T cells from the leukocytes of celiac disease patients in vitro. We also find elevated levels of KIR <jats:sup>+</jats:sup> CD8 <jats:sup>+</jats:sup> T cells, but not CD4 <jats:sup>+</jats:sup> regulatory T cells, in COVID-19 patients, correlating with disease severity and vasculitis. Selective ablation of Ly49 <jats:sup>+</jats:sup> CD8 <jats:sup>+</jats:sup> T cells in virus-infected mice led to autoimmunity after infection. Our results indicate that in both species, these regulatory CD8 <jats:sup>+</jats:sup> T cells act specifically to suppress pathogenic T cells in autoimmune and infectious diseases. </jats:p>

収録刊行物

  • Science

    Science 376 (6590), eabi9591-, 2022-04-15

    American Association for the Advancement of Science (AAAS)

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