Increased efficiency of binding of nascent C3b to the erythrocytes of chronic cold agglutinin disease.

Parker, Charles J.; Soldato, Cathy M.; Telen, Marilyn J.

doi:10.1172/jci111472

Cited by 35 publications

(26 citation statements)

References 23 publications

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“…With respect to the first possibility, immune complexes bearing fragments of C3 are present in patients with SLE (49), and these may interact with CR1 and CR2 to cause their removal from the cell surface, as has been demonstrated in vitro with receptor-specific antibodies (50,51). Secondary deficiencies of CR1 on erythrocytes have been shown to occur in SLE and in autoimmune hemolytic anemias in association with the generation of C3 cleavage fragments (6,7,52). The only previous demonstration of abnormalities in leukocyte CR 1 expression was in an SLE patient who had an autoantibody to this receptor (1 1).…”

Section: Discussionmentioning

confidence: 99%

Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus

Wilson

Ratnoff

Schur

et al. 1986

Arthritis & Rheumatism

165

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Decreased numbers of complement receptor type 1 (CR1) have been observed on erythrocytes of patients wilh systemic lupus erythematosus (SLE) and on glomerular podocytes of patients having proliferative nephritis of SLE. In the present study, the analysis of the cellular expression of CR1 has been extended to include leukocytes. In addition, expression by B lymphocytes of the C3d receptor (CR2), which also serves as the receptor for the Epstein-Barr virus, was assessed. Receptor expression was measured by 2-color fluorescent flow cytometry of peripheral blood B cells, identified by the presence of the B1 antigen, that had also been stained with anti-CR1 or anti-CR2. B cells from 17 patients with SLE exhibited a mean relative fluorescence for CR1 that was 61% of that found in 17 normal individuals (P < 0.001). The expression of CR2 by the patients' B cells (n = 14) was 62% of that of the B cells fraim normal subjects (n = 17) (P < 0.001). The expression of CR1 correlated with that of CR2 among patients (r = 0.63; P < 0.01) but not with the expression of CR2 among normal individuals (r = 0.36; P > 0.1).Thle mean CR1 content of the patients' neutrophils was only 59% of the normal mean (P < 0.001). Thus, abnormalities of complement receptor expression occur

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Section: Discussionmentioning

confidence: 99%

Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus

Wilson

Ratnoff

Schur

et al. 1986

Arthritis & Rheumatism

165

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“…In some experiments, the anti-C9 antibody was labeled with J2SI (Amersham, Arlington Heights, IL) using 1,3,4,6-tetrachloro-3a,6a-diphenylglycouril (Sigma) by the method of Parker et al (18). The radiolabeled ant ibodies (sp act, 8.8 x lOs cpmj Ilg)were dialyzed against three changes of PBS and stored at 4"C. Protein concentrations were determined spectrophotometrically (19,20).…”

Section: -----------------------mentioning

confidence: 99%

Supplemental Complement Component C9 Enhances the Capacity of Neonatal Serum to Kill Multiple Isolates of Pathogenic Escherichia coli

et al. 1994

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“…Erythrocytes from normal donors and from patients with chronic cold agglutinin disease (CCAD) (14) and PNH (7) were prepared and stored as previously described. The PNH II cells were obtained from a patient with 93% type II and 7% type III cells, whereas the PNH III cells were obtained from a patient with -88% type III and 12% type I cells (1,2).…”

Section: Methodsmentioning

confidence: 99%

“…Monoclonal anti-C3c as ascites fluid (Bethesda Research Laboratories, Gaithersburg, MD) was purified as previously described (7). Monoclonal anti-C3d (14), anti-C3dg (14), and anti-CR 1 (complement receptor type 1) (14) were gifts from Dr. Gordon D. Ross (University of North Carolina, Chapel Hill, NC). They were purified using 5% caprylic acid (Sigma Chemical Co.) (14).…”

Section: Methodsmentioning

confidence: 99%

“…Monoclonal anti-C3d (14), anti-C3dg (14), and anti-CR 1 (complement receptor type 1) (14) were gifts from Dr. Gordon D. Ross (University of North Carolina, Chapel Hill, NC). They were purified using 5% caprylic acid (Sigma Chemical Co.) (14). The anti-C3d was further purified by adsorption and elution (using 4 M MgCI2) from an affinity column bearing C3d.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of the complement sensitivity of paroxysmal nocturnal hemoglobinuria erythrocytes.

Parker¹,

Wiedmer²,

Sims³

et al. 1985

J. Clin. Invest.

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The affected erythrocytes of paroxysmal nocturnal hemoglobinuria (PNH II and PNH III cells) are abnormally sensitive to complement-mediated lysis. Normal human erythrocytes chemically modified by treatment with 2-amino-ethylisothiouronium bromide (AET) have been used as models for PNH cells inasmuch as they also exhibit an enhanced susceptibility to complement. To investigate the bases for the greater sensitivity of these abnormal cells to complement-mediated lysis, we compared binding of C3 and constituents of the membrane attack complex to normal, PNH II, PNH III, and AET-treated cells after classical pathway activation by antibody and fluidphase activation by cobra venom factor complexes. When whole serum complement was activated by antibody, there was increased binding of C3 and C9 to PNH II, PNH III, and AET-treated cells, although the binding of these complement components to PNH II and PNH III cells was considerably greater than their binding to the AET-treated cells. In addition, all of the abnormal cell types showed a greater degree of lysis per C9 bound than did the normal erythrocytes. PNH III and AET-treated cells were readily lysed by fluid-phase activation of complement, whereas normal and PNH II erythrocytes were not susceptible to bystander lysis. The greater hemolysis of PNH III and AET-treated cells in this reactive lysis system was due to a quantitative increase in binding of constituents of the membrane attack complex. This more efficient binding of the terminal components after fluid-phase activation of whole serum complement was not mediated by cell-bound C3 fragments. These investigations demonstrate that the molecular events that characterize the enhanced susceptibility of PNH II, PNH III, and AET-treated erythrocytes to complementmediated lysis are heterogeneous.

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Increased efficiency of binding of nascent C3b to the erythrocytes of chronic cold agglutinin disease.

Cited by 35 publications

References 23 publications

Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus

Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus

Supplemental Complement Component C9 Enhances the Capacity of Neonatal Serum to Kill Multiple Isolates of Pathogenic Escherichia coli

Characterization of the complement sensitivity of paroxysmal nocturnal hemoglobinuria erythrocytes.

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