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      NETosis: Sculpting tumor metastasis and immunotherapy

      1 , 2 , 3
      Immunological Reviews

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          Summary

          The process of neutrophil extracellular traps (NETs) formation, called NETosis, is a peculiar death modality of neutrophils, which was first observed as an immune response against bacterial infection. However, recent work has revealed the unique biology of NETosis in facilitating tumor metastatic process. Neutrophil extracellular traps released by the tumor microenvironment (TME) shield tumor cells from cytotoxic immunity, leading to impaired tumor clearance. Besides, tumor cells tapped by NETs enable to travel through vessels and subsequently seed distant organs. Targeted ablation of NETosis has been proven to be beneficial in potentiating the efficacy of cancer immunotherapy in the metastatic settings. This review outlines the impact of NETosis at almost all stages of tumor metastasis. Furthermore, understanding the multifaceted interplay between NETosis and the TME components is crucial for supporting the rational development of highly effective combination immunotherapeutic strategies with anti‐NETosis for patients with metastatic disease.

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          Neutrophil extracellular traps kill bacteria.

          Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
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            The evolving tumor microenvironment: From cancer initiation to metastatic outgrowth

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              Myeloid-derived suppressor cells in the era of increasing myeloid cell diversity

              Myeloid-derived suppressor cells (MDSCs) are pathologically activated neutrophils and monocytes with potent immunosuppressive activity. They are implicated in the regulation of immune responses in many pathological conditions and are closely associated with poor clinical outcomes in cancer. Recent studies have indicated key distinctions between MDSCs and classical neutrophils and monocytes, and, in this Review, we discuss new data on the major genomic and metabolic characteristics of MDSCs. We explain how these characteristics shape MDSC function and could facilitate therapeutic targeting of these cells, particularly in cancer and in autoimmune diseases. Additionally, we briefly discuss emerging data on MDSC involvement in pregnancy, neonatal biology and COVID-19.
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                Author and article information

                Contributors
                Journal
                Immunological Reviews
                Immunological Reviews
                0105-2896
                1600-065X
                January 2024
                September 15 2023
                January 2024
                : 321
                : 1
                : 263-279
                Affiliations
                [1 ] Department of Digestive Diseases 1 Cancer Hospital of China Medical University, Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute Shenyang China
                [2 ] Department of General Surgery The Affiliated Bozhou Hospital of Anhui Medical University Bozhou China
                [3 ] Department of Gastric Surgery Cancer Hospital of China Medical University, Cancer Hospital of Dalian University of Technology, Liaoning Cancer Hospital & Institute Shenyang China
                Article
                10.1111/imr.13277
                37712361
                16aac170-290f-420d-9e66-2e47e0a77c81
                © 2024

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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