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Sepsis-Induced Immunosuppression: The Role of Co-inhibitory Molecules

Received: 15 August 2024     Accepted: 26 August 2024     Published: 30 August 2024
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Abstract

Sepsis is one of the most common cause of death among hospitalized patients in the intensive care unit (ICU), with current therapeutic options falling short of a comprehensive solution. The condition's pathophysiology is marked by a spectrum of immunological impairments, with a growing consensus that immunosuppression plays a decisive role in the condition's rising morbidity and mortality rates. Extensive preclinical and clinical research has identified the upregulation of several co-inhibitory molecules during sepsis, including Programmed Death-1 (PD-1), Programmed Death Ligand-1 (PD-L1), Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4), B and T Lymphocyte Attenuator (BTLA), T Cell Membrane Protein-3 (TIM-3), and Lymphocyte Activation Gene-3 (LAG-3). These molecules, which exert a significant inhibitory effect on T cell function, are believed to contribute to the immunosuppressive state induced by sepsis. The elucidation of the intricate mechanisms by which these molecules induce immunosuppression is essential for devising the most efficacious treatment strategies for sepsis. The burgeoning field of immunotherapy, particularly the blockade of co-inhibitory molecules, represents a significant frontier in sepsis research. This approach holds substantial promise for the future of sepsis therapy, warranting further exploration and clinical investigation to harness its potential fully.

Published in Science Journal of Clinical Medicine (Volume 13, Issue 3)
DOI 10.11648/j.sjcm.20241303.13
Page(s) 57-62
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Sepsis, Immunosuppression, Co-inhibitory Molecules, PD-1, PD-L1, CTLA-4, BTLA, TIM -3, LAG-3, Immunotherapy

References
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Cite This Article
  • APA Style

    Zhao, D., Li, Y. (2024). Sepsis-Induced Immunosuppression: The Role of Co-inhibitory Molecules. Science Journal of Clinical Medicine, 13(3), 57-62. https://doi.org/10.11648/j.sjcm.20241303.13

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    ACS Style

    Zhao, D.; Li, Y. Sepsis-Induced Immunosuppression: The Role of Co-inhibitory Molecules. Sci. J. Clin. Med. 2024, 13(3), 57-62. doi: 10.11648/j.sjcm.20241303.13

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    AMA Style

    Zhao D, Li Y. Sepsis-Induced Immunosuppression: The Role of Co-inhibitory Molecules. Sci J Clin Med. 2024;13(3):57-62. doi: 10.11648/j.sjcm.20241303.13

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  • @article{10.11648/j.sjcm.20241303.13,
      author = {Dai-liang Zhao and Yan Li},
      title = {Sepsis-Induced Immunosuppression: The Role of Co-inhibitory Molecules
    },
      journal = {Science Journal of Clinical Medicine},
      volume = {13},
      number = {3},
      pages = {57-62},
      doi = {10.11648/j.sjcm.20241303.13},
      url = {https://doi.org/10.11648/j.sjcm.20241303.13},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sjcm.20241303.13},
      abstract = {Sepsis is one of the most common cause of death among hospitalized patients in the intensive care unit (ICU), with current therapeutic options falling short of a comprehensive solution. The condition's pathophysiology is marked by a spectrum of immunological impairments, with a growing consensus that immunosuppression plays a decisive role in the condition's rising morbidity and mortality rates. Extensive preclinical and clinical research has identified the upregulation of several co-inhibitory molecules during sepsis, including Programmed Death-1 (PD-1), Programmed Death Ligand-1 (PD-L1), Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4), B and T Lymphocyte Attenuator (BTLA), T Cell Membrane Protein-3 (TIM-3), and Lymphocyte Activation Gene-3 (LAG-3). These molecules, which exert a significant inhibitory effect on T cell function, are believed to contribute to the immunosuppressive state induced by sepsis. The elucidation of the intricate mechanisms by which these molecules induce immunosuppression is essential for devising the most efficacious treatment strategies for sepsis. The burgeoning field of immunotherapy, particularly the blockade of co-inhibitory molecules, represents a significant frontier in sepsis research. This approach holds substantial promise for the future of sepsis therapy, warranting further exploration and clinical investigation to harness its potential fully.
    },
     year = {2024}
    }
    

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    AU  - Yan Li
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    AB  - Sepsis is one of the most common cause of death among hospitalized patients in the intensive care unit (ICU), with current therapeutic options falling short of a comprehensive solution. The condition's pathophysiology is marked by a spectrum of immunological impairments, with a growing consensus that immunosuppression plays a decisive role in the condition's rising morbidity and mortality rates. Extensive preclinical and clinical research has identified the upregulation of several co-inhibitory molecules during sepsis, including Programmed Death-1 (PD-1), Programmed Death Ligand-1 (PD-L1), Cytotoxic T-Lymphocyte Antigen-4 (CTLA-4), B and T Lymphocyte Attenuator (BTLA), T Cell Membrane Protein-3 (TIM-3), and Lymphocyte Activation Gene-3 (LAG-3). These molecules, which exert a significant inhibitory effect on T cell function, are believed to contribute to the immunosuppressive state induced by sepsis. The elucidation of the intricate mechanisms by which these molecules induce immunosuppression is essential for devising the most efficacious treatment strategies for sepsis. The burgeoning field of immunotherapy, particularly the blockade of co-inhibitory molecules, represents a significant frontier in sepsis research. This approach holds substantial promise for the future of sepsis therapy, warranting further exploration and clinical investigation to harness its potential fully.
    
    VL  - 13
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