T cell exhaustion and Interleukin 2 downregulation |
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| Institution: | 1. Department of Medicine, Tufts Medical Center and Tufts University School of Medicine, Boston, MA, United States;2. Boston University Medical Center, Boston, MA, United States;1. Department of Immunology, University Hospital Zurich, University of Zurich, CH-8091 Zurich, Switzerland;1. Department of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA;2. Department of Information and Computer Science, Aalto University School of Science, Aalto 00076, Finland;3. Division of Rheumatology, Allergy, and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA;4. Department of Cancer Biology, The Scripps Research Institute, Jupiter, FL 33458, USA;5. Institute of Molecular Immunology, Helmholtz Zentrum München, Marchioninistrasse 25, 81377 Munich, Germany;6. Ludwig-Maximilians-Universität München, Institute for Immunology, Goethestrasse 31, 80336 Munich, Germany;7. Department of Radiology, St Lukes Roosevelt Hospital Center, New York, NY 10019, USA;8. Department of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA;9. Immune Disease Institute, Harvard Medical School and Program in Cellular and Molecular Medicine, Children’s Hospital Boston, Boston, MA 02115, USA;10. Department of Microbiology and Immunology, Sandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA 94143, USA;1. Department of Anatomy, School of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran;2. Department of Anatomy, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran;1. Laboratory of Viral Immunopathology, Unit of Infectious Diseases and Hepatology, Azienda Ospedaliero-Universitaria of Parma, Parma, Italy;2. Department of Medicine and Surgery, University of Parma, Parma, Italy;1. Department of Clinical Neurosciences and the Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada |
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| Abstract: | T cells reactive to tumor antigens and viral antigens lose their reactivity when exposed to the antigen-rich environment of a larger tumor bed or viral load. Such non-responsive T cells are termed exhausted. T cell exhaustion affects both CD8+ and CD4+ T cells. T cell exhaustion is attributed to the functional impairment of T cells to produce cytokines, of which the most important may be Interleukin 2 (IL2). IL2 performs functions critical for the elimination of cancer cells and virus infected cells. In one such function, IL2 promotes CD8+ T cell and natural killer (NK) cell cytolytic activities. Other functions include regulating naïve T cell differentiation into Th1 and Th2 subsets upon exposure to antigens. Thus, the signaling pathways contributing to T cell exhaustion could be linked to the signaling pathways contributing to IL2 loss. This review will discuss the process of T cell exhaustion and the signaling pathways that could be contributing to T cell exhaustion. |
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| Keywords: | T cells Exhaustion Interleukin 2 Chromatin PD1 |
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