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      Sessile Innate Immune Cells

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      2 ,
      Damage-Associated Molecular Patterns in Human Diseases

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          Abstract

          In this chapter, sessile cells of the innate immune system are briefly introduced. Defined as cells equipped with diverse pattern recognition molecules capable of detecting MAMPs and DAMPs, they encompass cells such as epithelial cells, fibroblasts, vascular cells, chondrocytes, osteoblasts, and adipocytes. Located at the body surfaces, epithelial cells represent the first line of innate immune defense against invading microbial pathogens. They are significant contributors to innate mucosal immunity and generate various antimicrobial defense mechanisms. Also, epithelial cells critically contribute to tissue repair via the phenomenon of re-epithelialization. Fibroblasts operate as classical sentinel cells of the innate immune system dedicated to responding to MAMPs and DAMPs emitted upon any tissue injury. Typically, fibroblasts synthesize most of the extracellular matrix of connective tissues, thereby playing a crucial role in tissue repair processes. Vascular cells of the innate immune system represent an evolutionarily developed first-line defense against any inciting insult hitting the vessel walls from the luminal side including bacteria, viruses, microbial toxins, and chemical noxa such as nicotine. Upon such insults and following recognition of MAMPs and DAMPs, vascular cells react with an innate immune response to create an acute inflammatory milieu in the vessel wall aimed at curing the vascular injury concerned. Chondrocytes, osteoblasts, and osteoclasts represent other vital cells of the skeletal system acting as cells of the innate immune system in its wider sense. These cells mediate injury-promoted DAMP-induced inflammatory and regenerative processes specific for the skeletal systems. Finally, adipocytes are regarded as highly active cells of the innate immune system. As white, brown, and beige adipocytes, they operate as a dynamic metabolic organ that can secrete certain bioactive molecules which have endocrine, paracrine, and autocrine actions.

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            Small populations of adult stem cells are responsible for the remarkable ability of the epithelial lining of the intestine to be efficiently renewed and repaired throughout life. The recent discovery of specific markers for these stem cells, together with the development of new technologies to track endogenous stem cell activity in vivo and to exploit their ability to generate new epithelia ex vivo, has greatly improved our understanding of stem cell-driven homeostasis, regeneration and cancer in the intestine. These exciting new insights into the biology of intestinal stem cells have the potential to accelerate the development of stem cell-based therapies and ameliorate cancer treatments.
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              Macrophage subsets in atherosclerosis.

              Macrophage accumulation within the vascular wall is a hallmark of atherosclerosis. In atherosclerotic lesions, macrophages respond to various environmental stimuli, such as modified lipids, cytokines, and senescent erythrocytes, which can modify their functional phenotypes. The results of studies on human atherosclerotic plaques demonstrate that the relative proportions of macrophage subsets within a plaque might be a better indicator of plaque phenotype and stability than the total number of macrophages. Understanding the function of specific macrophage subsets and their contribution to the composition and growth of atherosclerotic plaques would aid the identification of novel strategies to delay or halt the development of the disease and its associated pathophysiological consequences. However, most studies aimed at characterizing the phenotypes of human macrophages are performed in vitro and, therefore, their functional relevance to human pathology remains uncertain. In this Review, the diverse range of macrophage phenotypes in atherosclerotic lesions and their potential roles in both plaque progression and stability are discussed, with an emphasis on human pathology.
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                Author and article information

                Journal
                978-3-319-78655-1
                10.1007/978-3-319-78655-1
                Damage-Associated Molecular Patterns in Human Diseases
                Damage-Associated Molecular Patterns in Human Diseases
                Volume 1: Injury-Induced Innate Immune Responses
                978-3-319-78654-4
                978-3-319-78655-1
                28 March 2018
                : 159-186
                Affiliations
                GRID grid.11843.3f, ISNI 0000 0001 2157 9291, University of Strasbourg, , Molecular ImmunoRheumatology, Laboratory of Excellence Transplantex, ; Strasbourg, France
                Author information
                http://orcid.org/0000-0002-0090-0629
                Article
                9
                10.1007/978-3-319-78655-1_9
                7123606
                0e6d698d-f0e0-433e-8cfb-9758df2462dc
                © Springer International Publishing AG, part of Springer Nature 2018

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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                © Springer International Publishing AG, part of Springer Nature 2018

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