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      Trichuris suis induces human non-classical patrolling monocytes via the mannose receptor and PKC: implications for multiple sclerosis.

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          Abstract

          The inverse correlation between prevalence of auto-immune disorders like the chronic neuro-inflammatory disease multiple sclerosis (MS) and the occurrence of helminth (worm) infections, suggests that the helminth-trained immune system is protective against auto-immunity. As monocytes are regarded as crucial players in the pathogenesis of auto-immune diseases, we explored the hypothesis that these innate effector cells are prime targets for helminths to exert their immunomodulatory effects.

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          Most cited references41

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          Multiple sclerosis--the plaque and its pathogenesis.

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            The CD14+ CD16+ blood monocytes: their role in infection and inflammation.

            Blood monocyte subpopulations have been defined in man initially, and the two major types of monocytes are the CD14++ CD16- and the CD14+ CD16+ monocytes. These cells have been shown to exhibit distinct phenotype and function, and the CD14+ CD16+ were labeled proinflammatory based on higher expression of proinflammatory cytokines and higher potency in antigen presentation. The current review describes these properties, including the relationship to dendritic cells, and summarizes the host of publications about CD14+ CD16+ monocytes in inflammation and infectious disease in man, all of which suggest a crucial role of these cells in the disease processes. The review also covers the more recent description of homologues of these cells in other model species, which is expected to better define the role of monocyte subsets in disease.
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              The mannose receptor.

              The MR is a highly effective endocytic receptor with a broad binding specificity encompassing ligands of microbial and endogenous origin and a poorly characterized ability to modulate cellular activation. This review provides an update of the latest developments in the field. It discusses how MR biology might be affected by glycosylation and proteolytic processing, MR involvement in antigen delivery, and the potential contribution of MR to T cell differentiation and cellular activation. Further understanding of these areas will, no doubt, inform the design of novel, therapeutic tools for improved vaccination, control of inflammation, and tumor chemotherapy, which will benefit from exploiting MR-efficient internalization properties and unique pattern of expression.
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                Author and article information

                Journal
                Acta Neuropathol Commun
                Acta neuropathologica communications
                Springer Science and Business Media LLC
                2051-5960
                2051-5960
                Jul 25 2015
                : 3
                Affiliations
                [1 ] Department of Molecular Cell Biology and Immunology, Neuroscience Campus Amsterdam, VU University Medical Center, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands. G.kooij@vumc.nl.
                [2 ] Department of Molecular Cell Biology and Immunology, Neuroscience Campus Amsterdam, VU University Medical Center, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
                [3 ] Divison of Neonatology, Paediatric Intensive Care and Neuropaediatrics, Department of Paediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
                [4 ] CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
                [5 ] Hôpital Femme Mère Enfant, Hospices Civils de Lyon and Université de Lyon, Lyon, France.
                [6 ] Department of Blood Cell Research, University of Amsterdam, Amsterdam, The Netherlands.
                [7 ] Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
                [8 ] Department of Biochemistry, Emory University School of Medicine, Atlanta, USA.
                Article
                10.1186/s40478-015-0223-1
                10.1186/s40478-015-0223-1
                4513676
                26205402
                bcf15f40-7b32-4e2c-864b-6a3732dac565
                History

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