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      Complement Receptor 1: Disease associations and therapeutic implications

      review-article
      Author(s): , *
      Publication date (Electronic):
      Journal: Molecular Immunology
      Publisher: Elsevier Ltd. Published by Elsevier Ltd.
      Keywords: CR1, Complement Receptor 1, SLE, systemic lupus erythematosus, SARS, severe acute respiratory syndrome, sCR1, soluble Complement Receptor 1, uCR1, urinary Complement Receptor 1, SCR, short consensus repeats, LHR, long homologous repeats, PfEMP1, Plasmodiumfalciparum erythrocyte membrane protein 1, ECR1, erythrocyte Complement Receptor 1, kDa, kilo Dalton, RFLP, restriction fragment length polymorphism, SNP, single nucleotide polymorphism, LCR1, leukocyte Complement Receptor 1, Sl, Swain–Langley, McC, McCoy, HIV, human immunodeficiency virus, AIDS, acquired immunodeficiency syndrome, ESAT, early secreted antigen target, rCR1, recombinant Complement Receptor 1, TNFα, tumor necrosis factor α, TNFβ, tumor necrosis factor β, IL, interleukin, IFNγ, interferon γ, NCR1, neutrophil Complement Receptor 1, Complement Receptor 1, Review, Therapeutic implications, Complement genetics, Disease associations

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          Abstract

          Exaggerated complement activation is a key event in the pathogenesis of a range of autoimmune and inflammatory diseases. Complement Receptor 1 (CR1) has emerged as a molecule of immense interest in gaining insight to the susceptibility, pathophysiology, diagnosis, prognosis and therapy of such diseases. This review brings forth a composite view of the current understanding on the structure, functions, genetics, disease associations and therapeutic implications of CR1.

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          P. falciparum rosetting mediated by a parasite-variant erythrocyte membrane protein and complement-receptor 1.

          J A Rowe, J M Moulds, C Newbold … (1997)
          The factors determining disease severity in malaria are complex and include host polymorphisms, acquired immunity and parasite virulence. Studies in Africa have shown that severe malaria is associated with the ability of erythrocytes infected with the parasite Plasmodium falciparum to bind uninfected erythrocytes and form rosettes. The molecular basis of resetting is not well understood, although a group of low-molecular-mass proteins called rosettins have been described as potential parasite ligands. Infected erythrocytes also bind to endothelial cells, and this interaction is mediated by the parasite-derived variant erythrocyte membrane protein PfEMP1, which is encoded by the var gene family. Here we report that the parasite ligand for rosetting in a P. falciparum clone is PfEMP1, encoded by a specific var gene. We also report that complement-receptor 1 (CR1) on erythrocytes plays a role in the formation of rosettes and that erythrocytes with a common African CR1 polymorphism (S1(a-)) have reduced adhesion to the domain of PfEMP1 that binds normal erythrocytes. Thus we describe a new adhesive function for PfEMP1 and raise the possibility that CR1 polymorphisms in Africans that influence the interaction between erythrocytes and PfEMP1 may protect against severe malaria.
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            Complement Receptor 1/Cd35 Is a Receptor for Mannan-Binding Lectin

            Ionita Ghiran, Sergi Barbashov, Lloyd Klickstein … (2000)
            Mannan-binding lectin (MBL), a member of the collectin family, is known to have opsonic function, although identification of its cellular receptor has been elusive. Complement C1q, which is homologous to MBL, binds to complement receptor 1 (CR1/CD35), and thus we investigated whether CR1 also functions as the MBL receptor. Radioiodinated MBL bound to recombinant soluble CR1 (sCR1) that had been immobilized on plastic with an apparent equilibrium dissociation constant of 5 nM. N-acetyl-d-glucosamine did not inhibit sCR1–MBL binding, indicating that the carbohydrate binding site of MBL is not involved in binding CR1. C1q inhibited MBL binding to immobilized sCR1, suggesting that MBL and C1q might bind to the same or adjacent sites on CR1. MBL binding to polymorphonuclear leukocytes (PMNs) was associated positively with changes in CR1 expression induced by phorbol myristate acetate. Finally, CR1 mediated the adhesion of human erythrocytes to immobilized MBL and functioned as a phagocytic receptor on PMNs for MBL–immunoglobulin G opsonized bacteria. Thus, MBL binds to both recombinant sCR1 and cellular CR1, which supports the role of CR1 as a cellular receptor for the collectin MBL.
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              A human complement receptor 1 polymorphism that reduces Plasmodium falciparum rosetting confers protection against severe malaria.

              I Cockburn, M J Mackinnon, A. O'Donnell … (2004)
              Parasitized red blood cells (RBCs) from children suffering from severe malaria often adhere to complement receptor 1 (CR1) on uninfected RBCs to form clumps of cells known as "rosettes." Despite a well documented association between rosetting and severe malaria, it is controversial whether rosetting is a cause or a correlate of parasite virulence. CR1-deficient RBC show greatly reduced rosetting; therefore, we hypothesized that, if rosetting is a direct cause of malaria pathology, CR1-deficient individuals should be protected against severe disease. In this study, we show that RBC CR1 deficiency occurs in up to 80% of healthy individuals from the malaria-endemic regions of Papua New Guinea. This RBC CR1 deficiency is associated with polymorphisms in the CR1 gene and, unexpectedly, with alpha-thalassemia, a common genetic disorder in Melanesian populations. Analysis of a case-control study demonstrated that the CR1 polymorphisms and alpha-thalassemia independently confer protection against severe malaria. We have therefore identified CR1 as a new malaria resistance gene and provided compelling evidence that rosetting is an important parasite virulence phenotype that should be a target for drug and vaccine development.
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                Author and article information

                Contributors
                Nibhriti Das
                Journal
                Journal ID (nlm-ta): Mol Immunol
                Journal ID (iso-abbrev): Mol. Immunol
                Title: Molecular Immunology
                Publisher: Elsevier Ltd. Published by Elsevier Ltd.
                ISSN (Print): 0161-5890
                ISSN (Electronic): 1872-9142
                Publication date PMC-release: 11 November 2008
                Publication date (Print): February 2009
                Publication date (Electronic): 11 November 2008
                Volume: 46
                Issue: 5
                Pages: 761-772
                Affiliations
                Department of Biochemistry, All India Institute of Medical Sciences, New Delhi 110029, India
                Author notes
                [* ]Corresponding author. Tel.: +91 11 26593407; fax: +91 11 26588641. nibhriti@ 123456hotmail.com
                Article
                Publisher ID: S0161-5890(08)00676-7
                DOI: 10.1016/j.molimm.2008.09.026
                PMC ID: 7125513
                PubMed ID: 19004497
                SO-VID: 9a18a2ef-d931-4da9-93f8-a679ad3a5889
                Copyright © Copyright © 2008 Elsevier Ltd. Published by Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 13 August 2008
                Date revision received : 15 September 2008
                Date accepted : 15 September 2008
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: cr1, complement receptor 1,sle, systemic lupus erythematosus,sars, severe acute respiratory syndrome,scr1, soluble complement receptor 1,ucr1, urinary complement receptor 1,scr, short consensus repeats,lhr, long homologous repeats,pfemp1, plasmodiumfalciparum erythrocyte membrane protein 1,ecr1, erythrocyte complement receptor 1,kda, kilo dalton,rflp, restriction fragment length polymorphism,snp, single nucleotide polymorphism,lcr1, leukocyte complement receptor 1,sl, swain–langley,mcc, mccoy,hiv, human immunodeficiency virus,aids, acquired immunodeficiency syndrome,esat, early secreted antigen target,rcr1, recombinant complement receptor 1,tnfα, tumor necrosis factor α,tnfβ, tumor necrosis factor β,il, interleukin,ifnγ, interferon γ,ncr1, neutrophil complement receptor 1,complement receptor 1,review,therapeutic implications,complement genetics,disease associations
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: cr1, complement receptor 1, sle, systemic lupus erythematosus, sars, severe acute respiratory syndrome, scr1, soluble complement receptor 1, ucr1, urinary complement receptor 1, scr, short consensus repeats, lhr, long homologous repeats, pfemp1, plasmodiumfalciparum erythrocyte membrane protein 1, ecr1, erythrocyte complement receptor 1, kda, kilo dalton, rflp, restriction fragment length polymorphism, snp, single nucleotide polymorphism, lcr1, leukocyte complement receptor 1, sl, swain–langley, mcc, mccoy, hiv, human immunodeficiency virus, aids, acquired immunodeficiency syndrome, esat, early secreted antigen target, rcr1, recombinant complement receptor 1, tnfα, tumor necrosis factor α, tnfβ, tumor necrosis factor β, il, interleukin, ifnγ, interferon γ, ncr1, neutrophil complement receptor 1, complement receptor 1, review, therapeutic implications, complement genetics, disease associations

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