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      Immune modulation of some autoimmune diseases: the critical role of macrophages and neutrophils in the innate and adaptive immunity

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          Abstract

          Macrophages and neutrophils are key components involved in the regulation of numerous chronic inflammatory diseases, infectious disorders, and especially certain autoimmune disease. However, little is known regarding the contribution of these cells to the pathogenesis of autoimmune disorders. Recent studies have aimed to clarify certain important factors affecting the immunogenicity of these cells, including the type and dose of antigen, the microenvironment of the cell-antigen encounter, and the number, subset, and phenotype of these cells, which can prevent or induce autoimmune responses. This review highlights the role of macrophage subsets and neutrophils in injured tissues, supporting their cooperation during the pathogenesis of certain autoimmune diseases.

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          Netting neutrophils in autoimmune small-vessel vasculitis.

          Kai Kessenbrock, Markus Krumbholz, Ulf Schönermarck … (2009)
          Small-vessel vasculitis (SVV) is a chronic autoinflammatory condition linked to antineutrophil cytoplasm autoantibodies (ANCAs). Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO). Deposition of NETs in inflamed kidneys and circulating MPO-DNA complexes suggest that NET formation triggers vasculitis and promotes the autoimmune response against neutrophil components in individuals with SVV.
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            Biology of interleukin-10.

            Robert Sabat, Gerald Grütz, Katarzyna Warszawska … (2010)
            Interleukin (IL)-10 is the most important cytokine with anti-inflammatory properties besides TGF-β and IL-35. It is produced by activated immune cells, in particular monocytes/macrophages and T cell subsets including Tr1, Treg, and Th1 cells. IL-10 acts through a transmembrane receptor complex, which is composed of IL-10R1 and IL-10R2, and regulates the functions of many different immune cells. In monocytes/macrophages, IL-10 diminishes the production of inflammatory mediators and inhibits antigen presentation, although it enhances their uptake of antigens. Additionally, IL-10 plays an important role in the biology of B cells and T cells. The special physiological relevance of this cytokine lies in the prevention and limitation of over-whelming specific and unspecific immune reactions and, in consequence, of tissue damage. At the same time, IL-10 strengthens the "scavenger"-function and contributes to induced tolerance. This review provides an overview about the cellular sources, molecular mechanisms, effects, and biological role of IL-10. Copyright © 2010 Elsevier Ltd. All rights reserved.
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              Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities.

              Miriam Cnop, Nils Welsh, Jean-Christophe Jonas … (2005)
              Type 1 and type 2 diabetes are characterized by progressive beta-cell failure. Apoptosis is probably the main form of beta-cell death in both forms of the disease. It has been suggested that the mechanisms leading to nutrient- and cytokine-induced beta-cell death in type 2 and type 1 diabetes, respectively, share the activation of a final common pathway involving interleukin (IL)-1beta, nuclear factor (NF)-kappaB, and Fas. We review herein the similarities and differences between the mechanisms of beta-cell death in type 1 and type 2 diabetes. In the insulitis lesion in type 1 diabetes, invading immune cells produce cytokines, such as IL-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. IL-1beta and/or TNF-alpha plus IFN-gamma induce beta-cell apoptosis via the activation of beta-cell gene networks under the control of the transcription factors NF-kappaB and STAT-1. NF-kappaB activation leads to production of nitric oxide (NO) and chemokines and depletion of endoplasmic reticulum (ER) calcium. The execution of beta-cell death occurs through activation of mitogen-activated protein kinases, via triggering of ER stress and by the release of mitochondrial death signals. Chronic exposure to elevated levels of glucose and free fatty acids (FFAs) causes beta-cell dysfunction and may induce beta-cell apoptosis in type 2 diabetes. Exposure to high glucose has dual effects, triggering initially "glucose hypersensitization" and later apoptosis, via different mechanisms. High glucose, however, does not induce or activate IL-1beta, NF-kappaB, or inducible nitric oxide synthase in rat or human beta-cells in vitro or in vivo in Psammomys obesus. FFAs may cause beta-cell apoptosis via ER stress, which is NF-kappaB and NO independent. Thus, cytokines and nutrients trigger beta-cell death by fundamentally different mechanisms, namely an NF-kappaB-dependent mechanism that culminates in caspase-3 activation for cytokines and an NF-kappaB-independent mechanism for nutrients. This argues against a unifying hypothesis for the mechanisms of beta-cell death in type 1 and type 2 diabetes and suggests that different approaches will be required to prevent beta-cell death in type 1 and type 2 diabetes.
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                Author and article information

                Contributors
                Kely Campos Navegantes: kcnavegantes@gmail.com
                Rafaelli de Souza Gomes: rafaelli_gomes@hotmail.com
                Priscilla Aparecida Tártari Pereira: pritartari@yahoo.com.br
                Paula Giselle Czaikoski: paulimania@yahoo.com.br
                Carolina Heitmann Mares Azevedo: carolmheitmann@hotmail.com
                Marta Chagas Monteiro: +55 91 3201-7202 , martachagas2@yahoo.com.br
                Journal
                Journal ID (nlm-ta): J Transl Med
                Journal ID (iso-abbrev): J Transl Med
                Title: Journal of Translational Medicine
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1479-5876
                Publication date (Electronic): 15 February 2017
                Publication date PMC-release: 15 February 2017
                Publication date Collection: 2017
                Volume: 15
                Electronic Location Identifier: 36
                Affiliations
                [1 ]ISNI 0000 0001 2171 5249, GRID grid.271300.7, Pharmaceutical Science Post-Graduation Program, Health Science Institute, , Federal University of Pará/UFPA, ; Belém, PA 66075900 Brazil
                [2 ]Department of Clinical, Bromatological and Toxicological Analysis, Ribeirão Preto Pharmaceutical Sciences School, USP-SP, Ribeirão Preto, SP Brazil
                [3 ]GRID grid.466651.6, College of Pharmacy, , Guairacá Faculty-PR, ; Guarapuava, PR Brazil
                Article
                Publisher ID: 1141
                DOI: 10.1186/s12967-017-1141-8
                PMC ID: 5312441
                PubMed ID: 28202039
                SO-VID: 4c827a55-e7c8-4477-9dce-d0f64447ba49
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

                History
                Date received : 18 November 2016
                Date accepted : 3 February 2017
                Funding
                Funded by: CAPES
                Funded by: CNPQ
                Funded by: FAPESPA
                Funded by: FAPESP
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Medicine
                Keywords: macrophages,neutrophils,autoimmunity,autoimmune disease,inflammation
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: macrophages, neutrophils, autoimmunity, autoimmune disease, inflammation

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