title: CR1 on erythrocytes of Brazilian systemic lupus erythematosus patients: the influence of disease activity on expression and ability of this receptor to bind immune complexes opsonized with complement from normal human serum.
abstract: Hypocomplementaemia and low expression of CR1 on erythrocytes (E) of patients with systemic lupus erythematosus (SLE) are associated with defective clearance of circulating immune complexes (IC) and so they may have pathogenic significance. Here, we investigated whether the reduced CR1/E in SLE patients per se might affect the binding of IC to CR1/E. First, we analysed the expression of CR1 on E of active (n=30) and inactive (n=34) SLE patients using a FITC-conjugated mouse anti-CR1 monoclonal antibody E11 and flow cytometry. Both groups of patients had a significantly reduced CR1/E expression compared with healthy controls (n=40). It was also observed that the number of E bearing CR1 was reduced in both groups of SLE patients studied. Second, we determined the functional activity of CR1/E by measuring the binding to E of FITC-bovine serum albumin (BSA)/rabbit anti-BSA complexes, formed at equivalence, which were opsonized with complement from normal human serum (NHS). On the other hand, we did not find differences between the patient and control groups in the ability of E to bind IC/NHS. There was also a positive correlation between the CR1/E expression and the number of E bearing CR1 in control and inactive SLE groups, which was not observed in the group of active SLE patients. Considering the involvement of low levels of complement and CR1/E expression on complex processing, in this in vitro model the results show that an effective coating of the complexes with complement is sufficient to bind them preferentially to CR1 over normal levels of receptor expression.
authors.affiliation: Departamento de Física e Química, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Via do Café s/n, Monte Alegre, Ribeirão Preto, SP 14040-903, Brazil. clenimar@usp.br
authors.forename: C M
authors.initials: CM
authors.lastname: Marzocchi-Machado
authors.forename: C M O S
authors.initials: CM
authors.lastname: Alves
authors.forename: A E C S
authors.initials: AE
authors.lastname: Azzolini
authors.forename: A C M
authors.initials: AC
authors.lastname: Polizello
authors.forename: I F
authors.initials: IF
authors.lastname: Carvalho
authors.forename: Y M
authors.initials: YM
authors.lastname: Lucisano-Valim
mesh_terms: D000936:Antigen-Antibody Complex / Q000097:blood*; D001938:Brazil / Q000208:ethnology; D003165:Complement System Proteins / Q000378:metabolism*; D004912:Erythrocytes / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000208:ethnology / Q000276:immunology / Q000378:metabolism*; D009895:Opsonin Proteins / Q000097:blood*; D011485:Protein Binding / Q000276:immunology; D017463:Receptors, Complement 3b / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics*; D044967:Serum / Q000276:immunology / Q000378:metabolism
chemical_list: D000936:Antigen-Antibody Complex; D009895:Opsonin Proteins; D017463:Receptors, Complement 3b; D003165:Complement System Proteins