References
[1]. Yuki, K., & Koutsogiannaki, S. (2021). Pattern recognition receptors as therapeutic targets for bacterial, viral and fungal sepsis. International immunopharmacology, 98, 107909. Davis, A. R., Bush, C., Harvey, J. C. and Foley, M. F., "Fresnel lenses in rear projection displays," SID Int. Symp. Digest Tech. Papers 32(1), 934-937 (2001).
[2]. Huang, M., Cai, S., & Su, J. (2019). The Pathogenesis of Sepsis and Potential Therapeutic Targets. International journal of molecular sciences, 20(21), 5376.
[3]. Singer, M., Deutschman, C. S., Seymour, et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315(8), 801–810.
[4]. Gotts, J. E., & Matthay, M. A. (2016). Sepsis: pathophysiology and clinical management. BMJ (Clinical research ed.), 353, i1585.
[5]. Rimmelé, T., Payen, D., Cantaluppi, V., et al. (2016). IMMUNE CELL PHENOTYPE AND FUNCTION IN SEPSIS. Shock (Augusta, Ga.), 45(3), 282–291.
[6]. Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., Reece, J. B., & Campbell, N. A. (2018). Campbell Biology. Pearson Higher Education, Inc.
[7]. Venet, F., Monneret, G. Advances in the understanding and treatment of sepsis-induced immunosuppression. Nat Rev Nephrol 14, 121–137 (2018). Shhshs
[8]. Kasten, K. R., Tschöp, J., Goetzman, H. S., et al. (2010). T-cell activation differentially mediates the host response to sepsis. Shock (Augusta, Ga.), 34(4), 377–383.
[9]. Fazal, N., & Al-Ghoul, W. M. (2007). Thermal injury-plus-sepsis contributes to a substantial deletion of intestinal mesenteric lymph node CD4 T cell via apoptosis. International journal of biological sciences, 3(6), 393–401.
[10]. Huang, X., Venet, F., Wang, Y. L., et al. (2009). PD-1 expression by macrophages plays a pathologic role in altering microbial clearance and the innate inflammatory response to sepsis. Proceedings of the National Academy of Sciences of the United States of America, 106(15), 6303–6308.
[11]. Chen, J., Wang, H., Guo, R., Li, H., & Cui, N. (2022). Early Expression of Functional Markers on CD4+ T Cells Predicts Outcomes in ICU Patients With Sepsis. Frontiers in immunology, 13, 938538. Shshshs
[12]. Yan, L., Chen, Y., Han, Y., & Tong, C. (2022). Role of CD8+ T cell exhaustion in the progression and prognosis of acute respiratory distress syndrome induced by sepsis: a prospective observational study. BMC emergency medicine, 22(1), 182.
[13]. Guo, L., Shen, S., Rowley, J. W., et al. (2021). Platelet MHC class I mediates CD8+ T-cell suppression during sepsis. Blood, 138(5), 401–416.
[14]. Danahy, D. B., Strother, R. K., Badovinac, V. P., & Griffith, T. S. (2016). Clinical and Experimental Sepsis Impairs CD8 T-Cell-Mediated Immunity. Critical reviews in immunology, 36(1), 57–74.
[15]. Vignali, D. A., Collison, L. W., & Workman, C. J. (2008). How regulatory T cells work. Nature reviews. Immunology, 8(7), 523–532.
[16]. Nascimento, D. C., Melo, P. H., Piñeros, A. R., et al. (2017). IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nature communications, 8, 14919.
[17]. Gao, Y. L., Yao, Y., Zhang, X., et al. (2022). Regulatory T Cells: Angels or Demons in the Pathophysiology of Sepsis? Frontiers in immunology, 13, 829210.
[18]. Nalos, M., Santner-Nanan, B., Parnell, G., et al. (2012). Immune effects of interferon gamma in persistent staphylococcal sepsis. American journal of respiratory and critical care medicine, 185(1), 110–112.
[19]. Dyck, L., & Mills, K. H. G. (2017). Immune checkpoints and their inhibition in cancer and infectious diseases. European journal of immunology, 47(5), 765–779.
[20]. Astry, B., Venkatesha, S. H., Laurence, A., et al. (2015). Celastrol, a Chinese herbal compound, controls autoimmune inflammation by altering the balance of pathogenic and regulatory T cells in the target organ. Clinical immunology (Orlando, Fla.), 157(2), 228–238.
Cite this article
Zhang,M. (2023). T-cells’ roles and potentials as a therapeutic target in human sepsis. Theoretical and Natural Science,6,198-204.
Data availability
The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.
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References
[1]. Yuki, K., & Koutsogiannaki, S. (2021). Pattern recognition receptors as therapeutic targets for bacterial, viral and fungal sepsis. International immunopharmacology, 98, 107909. Davis, A. R., Bush, C., Harvey, J. C. and Foley, M. F., "Fresnel lenses in rear projection displays," SID Int. Symp. Digest Tech. Papers 32(1), 934-937 (2001).
[2]. Huang, M., Cai, S., & Su, J. (2019). The Pathogenesis of Sepsis and Potential Therapeutic Targets. International journal of molecular sciences, 20(21), 5376.
[3]. Singer, M., Deutschman, C. S., Seymour, et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315(8), 801–810.
[4]. Gotts, J. E., & Matthay, M. A. (2016). Sepsis: pathophysiology and clinical management. BMJ (Clinical research ed.), 353, i1585.
[5]. Rimmelé, T., Payen, D., Cantaluppi, V., et al. (2016). IMMUNE CELL PHENOTYPE AND FUNCTION IN SEPSIS. Shock (Augusta, Ga.), 45(3), 282–291.
[6]. Urry, L. A., Cain, M. L., Wasserman, S. A., Minorsky, P. V., Reece, J. B., & Campbell, N. A. (2018). Campbell Biology. Pearson Higher Education, Inc.
[7]. Venet, F., Monneret, G. Advances in the understanding and treatment of sepsis-induced immunosuppression. Nat Rev Nephrol 14, 121–137 (2018). Shhshs
[8]. Kasten, K. R., Tschöp, J., Goetzman, H. S., et al. (2010). T-cell activation differentially mediates the host response to sepsis. Shock (Augusta, Ga.), 34(4), 377–383.
[9]. Fazal, N., & Al-Ghoul, W. M. (2007). Thermal injury-plus-sepsis contributes to a substantial deletion of intestinal mesenteric lymph node CD4 T cell via apoptosis. International journal of biological sciences, 3(6), 393–401.
[10]. Huang, X., Venet, F., Wang, Y. L., et al. (2009). PD-1 expression by macrophages plays a pathologic role in altering microbial clearance and the innate inflammatory response to sepsis. Proceedings of the National Academy of Sciences of the United States of America, 106(15), 6303–6308.
[11]. Chen, J., Wang, H., Guo, R., Li, H., & Cui, N. (2022). Early Expression of Functional Markers on CD4+ T Cells Predicts Outcomes in ICU Patients With Sepsis. Frontiers in immunology, 13, 938538. Shshshs
[12]. Yan, L., Chen, Y., Han, Y., & Tong, C. (2022). Role of CD8+ T cell exhaustion in the progression and prognosis of acute respiratory distress syndrome induced by sepsis: a prospective observational study. BMC emergency medicine, 22(1), 182.
[13]. Guo, L., Shen, S., Rowley, J. W., et al. (2021). Platelet MHC class I mediates CD8+ T-cell suppression during sepsis. Blood, 138(5), 401–416.
[14]. Danahy, D. B., Strother, R. K., Badovinac, V. P., & Griffith, T. S. (2016). Clinical and Experimental Sepsis Impairs CD8 T-Cell-Mediated Immunity. Critical reviews in immunology, 36(1), 57–74.
[15]. Vignali, D. A., Collison, L. W., & Workman, C. J. (2008). How regulatory T cells work. Nature reviews. Immunology, 8(7), 523–532.
[16]. Nascimento, D. C., Melo, P. H., Piñeros, A. R., et al. (2017). IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nature communications, 8, 14919.
[17]. Gao, Y. L., Yao, Y., Zhang, X., et al. (2022). Regulatory T Cells: Angels or Demons in the Pathophysiology of Sepsis? Frontiers in immunology, 13, 829210.
[18]. Nalos, M., Santner-Nanan, B., Parnell, G., et al. (2012). Immune effects of interferon gamma in persistent staphylococcal sepsis. American journal of respiratory and critical care medicine, 185(1), 110–112.
[19]. Dyck, L., & Mills, K. H. G. (2017). Immune checkpoints and their inhibition in cancer and infectious diseases. European journal of immunology, 47(5), 765–779.
[20]. Astry, B., Venkatesha, S. H., Laurence, A., et al. (2015). Celastrol, a Chinese herbal compound, controls autoimmune inflammation by altering the balance of pathogenic and regulatory T cells in the target organ. Clinical immunology (Orlando, Fla.), 157(2), 228–238.