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      Innate Immune Cells' Contribution to Systemic Lupus Erythematosus

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          Abstract

          Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the presence of autoantibodies against nuclear antigens, immune complex deposition, and tissue damage in the kidneys, skin, heart and lung. Because of the pathogenic role of antinuclear antibodies and autoreactive T cells in SLE, extensive efforts have been made to demonstrate how B cells act as antibody-producing or as antigen-presenting cells that can prime autoreactive T cell activation. With the discovery of new innate immune cells and inflammatory mediators, innate immunity is emerging as a key player in disease pathologies. Recent work over the last decade has highlighted the importance of innate immune cells and molecules in promoting and potentiating SLE. In this review, we discuss recent evidence of the involvement of different innate immune cells and pathways in the pathogenesis of SLE. We also discuss new therapeutics targets directed against innate immune components as potential novel therapies in SLE.

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          Most cited references78

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          The complement system

          The complement system consists of a tightly regulated network of proteins that play an important role in host defense and inflammation. Complement activation results in opsonization of pathogens and their removal by phagocytes, as well as cell lysis. Inappropriate complement activation and complement deficiencies are the underlying cause of the pathophysiology of many diseases such as systemic lupus erythematosus and asthma. This review represents an overview of the complement system in an effort to understand the beneficial as well as harmful roles it plays during inflammatory responses.
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            Induction of dendritic cell differentiation by IFN-alpha in systemic lupus erythematosus.

            Dendritic cells (DCs) are important in regulating both immunity and tolerance. Hence, we hypothesized that systemic lupus erythematosus (SLE), an autoimmune disease characterized by autoreactive B and T cells, may be caused by alterations in the functions of DCs. Consistent with this, monocytes from SLE patients' blood were found to function as antigen-presenting cells, in vitro. Furthermore, serum from SLE patients induced normal monocytes to differentiate into DCs. These DCs could capture antigens from dying cells and present them to CD4-positive T cells. The capacity of SLE patients' serum to induce DC differentiation correlated with disease activity and depended on the actions of interferon-alpha (IFN-alpha). Thus, unabated induction of DCs by IFN-alpha may drive the autoimmune response in SLE.
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              Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies.

              The complement system plays a paradoxical role in the development and expression of autoimmunity in humans. The activation of complement in systemic lupus erythematosus (SLE) contributes to tissue injury. In contrast, inherited deficiency of classical pathway components, particularly C1q (ref. 1), is powerfully associated with the development of SLE. This leads to the hypothesis that a physiological action of the early part of the classical pathway protects against the development of SLE (ref. 2) and implies that C1q may play a key role in this respect. C1q-deficient (C1qa-/-) mice were generated by gene targeting and monitored for eight months. C1qa-/- mice had increased mortality and higher titres of autoantibodies, compared with strain-matched controls. Of the C1qa-/- mice, 25% had glomerulonephritis with immune deposits and multiple apoptotic cell bodies. Among mice without glomerulonephritis, there were significantly greater numbers of glomerular apoptotic bodies in C1q-deficient mice compared with controls. The phenotype associated with C1q deficiency was modified by background genes. These findings are compatible with the hypothesis that C1q deficiency causes autoimmunity by impairment of the clearance of apoptotic cells.
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                Author and article information

                Contributors
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                15 April 2019
                2019
                : 10
                : 772
                Affiliations
                [1] 1Lymphatic and Inflammation Research Laboratory, Facultad de Ciencias de la Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile , Talca, Chile
                [2] 2Departamento de Inmunología Clínica y Reumatología, Escuela de Medicina, Pontificia Universidad Católica de Chile , Santiago, Chile
                [3] 3Laboratorio de Enfermedades Autoinmunes Oculares y Sistémicas, Departamento de Oftalmología, Facultad de Medicina, Universidad de Chile , Santiago, Chile
                [4] 4Departamento de Ciencias Químicas y Biológicas, Facultad de Salud, Universidad Bernardo O'Higgins , Santiago, Chile
                [5] 5Servicio de Oftalmología, Hospital Clínico Universidad de Chile , Santiago, Chile
                Author notes

                Edited by: J. Michelle Kahlenberg, University of Michigan, United States

                Reviewed by: Xin M. Luo, Virginia Tech, United States; Julia Weinmann-Menke, Johannes Gutenberg University Mainz, Germany

                *Correspondence: Loreto Cuitino cuitinole@ 123456gmail.com

                This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology

                Article
                10.3389/fimmu.2019.00772
                6476281
                31037070
                96af7e4a-0052-4770-93c9-4dbbd17a4cf0
                Copyright © 2019 Herrada, Escobedo, Iruretagoyena, Valenzuela, Burgos, Cuitino and Llanos.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 22 January 2019
                : 25 March 2019
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 103, Pages: 9, Words: 7085
                Funding
                Funded by: Comisión Nacional de Investigación Científica y Tecnológica 10.13039/501100002848
                Categories
                Immunology
                Mini Review

                Immunology
                lupus (sle),innate immunity,dendritic cells,macrophage-cell,innate lymphoid cell
                Immunology
                lupus (sle), innate immunity, dendritic cells, macrophage-cell, innate lymphoid cell

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