For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
6
views
236
references
 Top references
cited by
7
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      516
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Targeting cGAS/STING signaling-mediated myeloid immune cell dysfunction in TIME

      review-article
      Author(s): 1 , , 1 , 1 , 2 , 3 ,
      Publication date (Electronic):
      Journal: Journal of Biomedical Science
      Publisher: BioMed Central
      Keywords: Cancer, cGAS, STING, MIC, Macrophages, DCs, MDSCs, TME, TIME

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Myeloid immune cells (MICs) are potent innate immune cells serving as first responders to invading pathogens and internal changes to cellular homeostasis. Cancer is a stage of altered cellular homeostasis that can originate in response to different pathogens, chemical carcinogens, and internal genetic/epigenetic changes. MICs express several pattern recognition receptors (PRRs) on their membranes, cytosol, and organelles, recognizing systemic, tissue, and organ-specific altered homeostasis. cGAS/STING signaling is a cytosolic PRR system for identifying cytosolic double-stranded DNA (dsDNA) in a sequence-independent but size-dependent manner. The longer the cytosolic dsDNA size, the stronger the cGAS/STING signaling activation with increased type 1 interferon (IFN) and NF-κB-dependent cytokines and chemokines’ generation. The present article discusses tumor-supportive changes occurring in the tumor microenvironment (TME) or tumor immune microenvironment (TIME) MICs, specifically emphasizing cGAS/STING signaling-dependent alteration. The article further discusses utilizing MIC-specific cGAS/STING signaling modulation as critical tumor immunotherapy to alter TIME.

          Related collections

          Most cited references236

          • Record: found
          • Abstract: found
          • Article: not found

          Inflammation and cancer.

          Lisa Coussens, Zena Werb (2002)
          Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
          Article 0 comments Cited 1853 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Macrophage plasticity and polarization: in vivo veritas.

            Antonio Sica, Alberto Mantovani (2012)
            Diversity and plasticity are hallmarks of cells of the monocyte-macrophage lineage. In response to IFNs, Toll-like receptor engagement, or IL-4/IL-13 signaling, macrophages undergo M1 (classical) or M2 (alternative) activation, which represent extremes of a continuum in a universe of activation states. Progress has now been made in defining the signaling pathways, transcriptional networks, and epigenetic mechanisms underlying M1-M2 or M2-like polarized activation. Functional skewing of mononuclear phagocytes occurs in vivo under physiological conditions (e.g., ontogenesis and pregnancy) and in pathology (allergic and chronic inflammation, tissue repair, infection, and cancer). However, in selected preclinical and clinical conditions, coexistence of cells in different activation states and unique or mixed phenotypes have been observed, a reflection of dynamic changes and complex tissue-derived signals. The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for macrophage-centered diagnostic and therapeutic strategies.
            Article 0 comments Cited 1175 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Macrophages as regulators of tumour immunity and immunotherapy

              David DeNardo, Brian Ruffell (2019)
              Macrophages are critical mediators of tissue homeostasis, with tumors distorting this proclivity to stimulate proliferation, angiogenesis, and metastasis. This had led to an interest in targeting macrophages in cancer, and preclinical studies have demonstrated efficacy across therapeutic modalities and tumor types. Much of the observed efficacy can be traced to the suppressive capacity of macrophages, driven by microenvironmental cues such as hypoxia and fibrosis. As a result, tumor macrophages display an ability to suppress T cell recruitment and function as well as regulate other aspects of tumor immunity. With the increasing impact of cancer immunotherapy, macrophage targeting is now being evaluated in this context. Here we will discuss the results of clinical trials and the future of combinatorial immunotherapy.
              Article 0 comments Cited 841 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Vijay Kumar:
                ORCID: http://orcid.org/0000-0001-9741-3597
                vkuma2@lsuhsc.edu , vij_tox@yahoo.com
                John H. Stewart IV: jste17@lsuhsc.edu
                Journal
                Journal ID (nlm-ta): J Biomed Sci
                Journal ID (iso-abbrev): J Biomed Sci
                Title: Journal of Biomedical Science
                Publisher: BioMed Central (London )
                ISSN (Print): 1021-7770
                ISSN (Electronic): 1423-0127
                Publication date (Electronic): 28 June 2023
                Publication date PMC-release: 28 June 2023
                Publication date Collection: 2023
                Volume: 30
                Electronic Location Identifier: 48
                Affiliations
                [1 ]GRID grid.279863.1, ISNI 0000 0000 8954 1233, Department of Interdisciplinary Oncology, Stanley S. Scott Cancer Center, School of Medicine, , Louisiana State University Health Science Center (LSUHSC), ; 1700 Tulane Avenue, New Orleans, LA 70012 USA
                [2 ]GRID grid.279863.1, ISNI 0000 0000 8954 1233, Louisiana Children’s Medical Center Cancer Center, Stanley S. Scott Cancer Center, School of Medicine, , Louisiana State University Health Science Center (LSUHSC), ; 1700 Tulane Avenue, New Orleans, LA 70012 USA
                [3 ]GRID grid.279863.1, ISNI 0000 0000 8954 1233, Surgery, Section of Surgical Oncology, Louisiana State University New Orleans-Louisiana Children’s Medical Center Cancer Center, , Louisiana State University Health Science Center (LSUHSC), ; 1700 Tulane Avenue, New Orleans, LA 70012 USA
                Author information
                http://orcid.org/0000-0001-9741-3597
                Article
                Publisher ID: 942
                DOI: 10.1186/s12929-023-00942-2
                PMC ID: 10304357
                PubMed ID: 37380989
                SO-VID: 5ad0722f-b70f-4680-9fa8-c61145a4edb9
                Copyright © © The Author(s) 2023
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 3 April 2023
                Date accepted : 14 June 2023
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © National Science Council of the Republic of China (Taiwan) 2023

                ScienceOpen disciplines: Molecular medicine
                Keywords: cancer,cgas,sting,mic,macrophages,dcs,mdscs,tme,time
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: cancer, cgas, sting, mic, macrophages, dcs, mdscs, tme, time

                Comments

                Comment on this article

                scite_

                Similar content516

                See all similar

                Cited by7

                See all cited by

                Most referenced authors3,514

                See all reference authors