Complement in Non-Antibody-Mediated Kidney Diseases

The complement system is part of the innate immune response that plays important roles in protecting the host from foreign pathogens. The complement components and relative fragment deposition have long been recognized to be strongly involved also in the pathogenesis of autoantibody-related kidney g...

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Main Authors: Andrea Angeletti, Joselyn Reyes-Bahamonde, Paolo Cravedi, Kirk N. Campbell
Format: Article
Language:English
Published: Frontiers Media S.A. 2017-07-01
Series:Frontiers in Medicine
Subjects:
Online Access:http://journal.frontiersin.org/article/10.3389/fmed.2017.00099/full
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author Andrea Angeletti
Andrea Angeletti
Joselyn Reyes-Bahamonde
Paolo Cravedi
Kirk N. Campbell
author_facet Andrea Angeletti
Andrea Angeletti
Joselyn Reyes-Bahamonde
Paolo Cravedi
Kirk N. Campbell
author_sort Andrea Angeletti
collection DOAJ
description The complement system is part of the innate immune response that plays important roles in protecting the host from foreign pathogens. The complement components and relative fragment deposition have long been recognized to be strongly involved also in the pathogenesis of autoantibody-related kidney glomerulopathies, leading to direct glomerular injury and recruitment of infiltrating inflammation pathways. More recently, unregulated complement activation has been shown to be associated with progression of non-antibody-mediated kidney diseases, including focal segmental glomerulosclerosis, C3 glomerular disease, thrombotic microangiopathies, or general fibrosis generation in progressive chronic kidney diseases. Some of the specific mechanisms associated with complement activation in these diseases were recently clarified, showing a dominant role of alternative activation pathway. Over the last decade, a growing number of anticomplement agents have been developed, and some of them are being approved for clinical use or already in use. Therefore, anticomplement therapies represent a realistic choice of therapeutic approaches for complement-related diseases. Herein, we review the complement system activation, regulatory mechanisms, their involvement in non-antibody-mediated glomerular diseases, and the recent advances in complement-targeting agents as potential therapeutic strategies.
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spelling doaj.art-3b24b2716e2e4b0099e678197c45e1b32022-12-21T18:20:44ZengFrontiers Media S.A.Frontiers in Medicine2296-858X2017-07-01410.3389/fmed.2017.00099277857Complement in Non-Antibody-Mediated Kidney DiseasesAndrea Angeletti0Andrea Angeletti1Joselyn Reyes-Bahamonde2Paolo Cravedi3Kirk N. Campbell4Department of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY, United StatesDepartment of Experimental Diagnostic and Specialty Medicine (DIMES), Nephrology, Dialysis and Renal Transplant Unit, St Orsola Hospital, University of Bologna, Bologna, ItalyDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY, United StatesDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY, United StatesDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY, United StatesThe complement system is part of the innate immune response that plays important roles in protecting the host from foreign pathogens. The complement components and relative fragment deposition have long been recognized to be strongly involved also in the pathogenesis of autoantibody-related kidney glomerulopathies, leading to direct glomerular injury and recruitment of infiltrating inflammation pathways. More recently, unregulated complement activation has been shown to be associated with progression of non-antibody-mediated kidney diseases, including focal segmental glomerulosclerosis, C3 glomerular disease, thrombotic microangiopathies, or general fibrosis generation in progressive chronic kidney diseases. Some of the specific mechanisms associated with complement activation in these diseases were recently clarified, showing a dominant role of alternative activation pathway. Over the last decade, a growing number of anticomplement agents have been developed, and some of them are being approved for clinical use or already in use. Therefore, anticomplement therapies represent a realistic choice of therapeutic approaches for complement-related diseases. Herein, we review the complement system activation, regulatory mechanisms, their involvement in non-antibody-mediated glomerular diseases, and the recent advances in complement-targeting agents as potential therapeutic strategies.http://journal.frontiersin.org/article/10.3389/fmed.2017.00099/fullcomplement systemglomerular diseasethrombotic microangiopathyfibrosisfocal segmental glomerulosclerosis
spellingShingle Andrea Angeletti
Andrea Angeletti
Joselyn Reyes-Bahamonde
Paolo Cravedi
Kirk N. Campbell
Complement in Non-Antibody-Mediated Kidney Diseases
Frontiers in Medicine
complement system
glomerular disease
thrombotic microangiopathy
fibrosis
focal segmental glomerulosclerosis
title Complement in Non-Antibody-Mediated Kidney Diseases
title_full Complement in Non-Antibody-Mediated Kidney Diseases
title_fullStr Complement in Non-Antibody-Mediated Kidney Diseases
title_full_unstemmed Complement in Non-Antibody-Mediated Kidney Diseases
title_short Complement in Non-Antibody-Mediated Kidney Diseases
title_sort complement in non antibody mediated kidney diseases
topic complement system
glomerular disease
thrombotic microangiopathy
fibrosis
focal segmental glomerulosclerosis
url http://journal.frontiersin.org/article/10.3389/fmed.2017.00099/full
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