What's New in Shock, June 2021?
What's New in Shock, June 2021?
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2021 年 6 月《震撼》有哪些新内容?
DOI:
10.1097/shk.0000000000001800
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发表时间:
2021
期刊:
影响因子:
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通讯作者:
Kozar,RosemaryA
中科院分区:
文献类型:
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作者:
Zeineddin,Ahmad;Dong,Jing-Fei;Wu,Feng;Terse,Pranaya;Kozar,RosemaryA
It is our honor to author the June,“What's New in Shock” commentary as we have the privilege of reviewing an article from a longtime Shock member, Dr Michael Dubick, who recently passed. We thank him for his dedication to Shock as well as his many important contributions to science.As sepsis remains a disease with high mortality and an important focus of our journal, this month we discuss several articles on sepsis, with an emphasis on innate immunity. Trauma and sepsis are disease states that lead to persistent inflammation, immune suppression, and catabolism syndrome (PICS). While the acute inflammatory response that follows sepsis and trauma is well studied, the mechanisms governing prolonged immunosuppression are largely not understood. In this issue, Bergmann et al.(1) provide an extensive review on the contribution of lymphocytes to the development of PICS. The authors suggest that the imbalance of regulatory T cell (Tregs) subsets determines the development of immunosuppression. They then explain how Tregs, innate lymphoid cells, natural killer T cells, TCR-a CD4 CD8 double-negative T cells, and B cells participate in the development of immune dysfunction in trauma and sepsis. In particular, the contribution of regulatory B cells and the cytokines, interleukin-10 (IL-10), transforming growth factor beta, and IFN-g is discussed. While there is still no approved drug for the treatment of immune dysfunction, the following were suggested as important to therapy development and immune-phenotyping: intensive care unit dynamic immune monitoring, determination of immunologic states using a panel of biomarkers and functional assays, description of patient subgroups based on immune status, and consideration of repurposing autoimmune and cancer drugs for treatment of immune dysfunction following trauma and sepsis.