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      Role of macrophages in malignancy

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          Abstract

          Macrophages themselves are a heterogeneous mixture of cells which mediate their effects not only through phagocytosis but also through the production of various soluble factors such as cytokines and chemokines. The most important function of macrophages is the defense of the body against pathogen aggressions. However, when recruited within neoplastic tissues, tumor-associated macrophages polarize differently and do not predominantly exert their immune function but rather favor tumor growth and angiogenesis.

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          Regulation of the Chemokine Receptor CXCR4 by Hypoxia

          Tiziana Schioppa, Badarch Uranchimeg, Alessandra Saccani … (2003)
          Cell adaptation to hypoxia (Hyp) requires activation of transcriptional programs that coordinate expression of genes involved in oxygen delivery (via angiogenesis) and metabolic adaptation (via glycolysis). Here, we describe that oxygen availability is a determinant parameter in the setting of chemotactic responsiveness to stromal-derived factor 1 (CXCL12). Low oxygen concentration induces high expression of the CXCL12 receptor, CXC receptor 4 (CXCR4), in different cell types (monocytes, monocyte-derived macrophages, tumor-associated macrophages, endothelial cells, and cancer cells), which is paralleled by increased chemotactic responsiveness to its specific ligand. CXCR4 induction by Hyp is dependent on both activation of the Hyp-inducible factor 1 α and transcript stabilization. In a relay multistep navigation process, the Hyp–Hyp-inducible factor 1 α–CXCR4 pathway may regulate trafficking in and out of hypoxic tissue microenvironments.
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            Dual role of macrophages in tumor growth and angiogenesis.

            Chrystelle Lamagna, Michel Aurrand-Lions, Beat Imhof (2006)
            During the neoplastic progression, macrophages as well as dendritic and NK cells are attracted into the tumor site and initiate the immune response against transformed cells. They activate and present tumor antigens to T cells, which are then activated to kill tumor cells. However, tumor cells are often capable of escaping the immune machinery. As the immune surveillance is not sufficient anymore, tumor-associated macrophages contribute to tumor progression. It is notable that tumor-associated macrophages promote the proliferation of tumor cells directly by secreting growth factors. They also participate in tumor progression by acting on endothelial cells and thus promoting the neovascularization of the tumor. Tumor-associated macrophages are indeed key protagonists during angiogenesis and promote each step of the angiogenesis cascade.
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              Helicobacter pylori Modulates the T Helper Cell 1/T Helper Cell 2 Balance through Phase-variable Interaction between Lipopolysaccharide and DC-SIGN

              Mathijs P. Bergman, Anneke Engering, Hermelijn Smits … (2004)
              The human gastric pathogen Helicobacter pylori spontaneously switches lipopolysaccharide (LPS) Lewis (Le) antigens on and off (phase-variable expression), but the biological significance of this is unclear. Here, we report that Le+ H. pylori variants are able to bind to the C-type lectin DC-SIGN and present on gastric dendritic cells (DCs), and demonstrate that this interaction blocks T helper cell (Th)1 development. In contrast, Le− variants escape binding to DCs and induce a strong Th1 cell response. In addition, in gastric biopsies challenged ex vivo with Le+ variants that bind DC-SIGN, interleukin 6 production is decreased, indicative of increased immune suppression. Our data indicate a role for LPS phase variation and Le antigen expression by H. pylori in suppressing immune responses through DC-SIGN.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Maxillofac Surg
                Journal ID (iso-abbrev): Ann Maxillofac Surg
                Journal ID (publisher-id): AMS
                Title: Annals of Maxillofacial Surgery
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2231-0746
                ISSN (Electronic): 2249-3816
                Publication date (Print): Jul-Dec 2011
                Volume: 1
                Issue: 2
                Pages: 150-154
                Affiliations
                [1]Department of Oral Pathology and Microbiology, M. A. Rangoonwala's College of Dental Sciences and Research Centre, Azam Campus, Pune, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Gauri S. Dhabekar, M. A. Rangoonwala's College of Dental Sciences and Research Centre, Azam Campus, Pune – 01, Maharashtra, India. E-mail: gauri.dhabekar@ 123456gmail.com
                Article
                Publisher ID: AMS-1-150
                DOI: 10.4103/2231-0746.92782
                PMC ID: 3591014
                PubMed ID: 23482819
                SO-VID: a1007f41-46c2-446b-b1bd-95849e66c5f8
                Copyright © Copyright: © Annals of Maxillofacial Surgery
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Review Article

                Keywords: macrophages,cancer,tumor associated marcophages
                Data availability:
                Keywords: macrophages, cancer, tumor associated marcophages

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