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PubMed1987

Competitive enzyme-linked immunoassay for the quantitation of platelet-associated immunoglobulins (IgG, IgM, IgA) and complement (C3c, C3d) with polyclonal and monoclonal reagents.

A competitive enzyme-linked immunoassay (CELIA) was developed for the quantitation of platelet-associated immunoglobulins and complement proteins. The use of unlabeled polyclonal rabbit or monoclonal antibodies to human immunoglobulins and enzyme-labeled anti-mouse or anti--rabbit IgG (double-step technique) resulted in a higher sensitivity compared to the single-step technique using only enzyme-labeled anti-human immunoglobulin antibody preparations. Sensitivity and results obtained by both techniques were compared. The range of normal values for platelet-associated IgG, IgM, IgA, C3c and C3d was assessed upon a large number of normal blood donors. When platelet-associated IgG was concomitantly assayed with polyclonal and monoclonal anti-IgG by the double-step technique on platelets obtained from normal donors and thrombocytopenic patients, identical results were obtained with both reagents. Problems related to the quantitation of immunoglobulins on platelets with different assays and antibody preparations are discussed.

Antibodies, Monoclonal↗
PubMed1990

Reduction of complement activation during bypass by prime manipulation.

Complement activation is believed to be of importance in the development of complications arising after cardiopulmonary bypass. The effect on complement activation of priming the extracorporeal circuit with crystalloid alone, crystalloid plus albumin, or crystalloid plus the plasma expander polygeline was assessed in 36 patients undergoing coronary artery operations with cardiopulmonary bypass using a bubble oxygenator. Activation of the alternative and common complement pathways was monitored before, during, and after the bypass period by measuring concentrations of factor B and its fragment Ba and C3 and its fragment C3d. Complement activation occurred in all three groups of patients, with no difference between the crystalloid and crystalloid-albumin groups. In contrast, Ba fragment concentrations were persistently and significantly lower during and after bypass in the polygeline group, denoting reduced complement activation. C3d levels also showed a tendency to be lower in this group. Our results indicate that addition of polygeline to the priming solution reduces complement activation. Because complement activation is associated with morbidity after cardiopulmonary bypass, addition of polygeline to the priming solution may offer an inexpensive method of reducing morbidity after cardiopulmonary bypass.

Albumins↗
PubMed1990

Comparative study of assays detecting complement activation. Complement-split product C3d (rocket immuno-electrophoresis) and C3d neodeterminants (ELISA).

The aim of the study was to investigate the correlation between two types of assay measuring specific products of complement C3 activation and their clinical application. Complement C3d split product was estimated using double-decker rocket immunoelectrophoresis (DD-RIE) and measurements of C3d neodeterminants exposed after C3 activation was carried out with an enzyme-linked immunosorbent assay (ELISA). A total of 595 blood samples were measured in parallel in the DD-RIE and the ELISA test systems. The samples originated from blood donors (44), uraemic patients undergoing dialysis (135), serial samples from rheumatoid arthritis (RA) patients during steroid treatment (88) and 328 randomly collected patient samples. The mean values for DD-RIE and ELISA (+/- 1 SD) for the 595 samples were 48 (+/- 20) mU/l and 48 (+/- 28) mU/l respectively. The interassay coefficient of variation (CV) in the ELISA was 18%. The Spearman rho-correlation coefficient between the two assays was 0.63 for all 595 samples. The mean values using ELISA and DD-RIE were practically identical for the 328 successively incoming samples, the samples from the 135 dialysis patients and the 44 donors. In RA patients a higher mean value was found for the 88 samples using DD-RIE than ELISA. In the majority of patient samples there was a good correlation between the two assays. However, the ELISA appears to be more sensitive in detecting acute complement activation and to give lower levels in RA patients with chronic complement activation.

Anaphylaxis↗
PubMed1985

Mapping of the C3d receptor (CR2)-binding site and a neoantigenic site in the C3d domain of the third component of complement.

The C3d domain of C3 contains the site that binds to the C3d receptor (CR2) which is expressed on B lymphocytes. It also contains a neoantigenic determinant that is recognized by monoclonal antibody (mAb) 130 and is expressed when C3b is cleaved to iC3b and subsequently to C3dg or C3d. mAb 130 inhibits the binding of C3d to CR2. In this study, the locations of the CR2-binding site and of the neoantigen recognized by mAb 130 within the C3d domain were investigated. Treatment of human C3d with CNBr generated two major fragments with Mrs of 12,500 and 8600. Binding studies showed that only the Mr 8600 fragment was capable of binding to both CR2 and mAb 130. Amino-terminal sequence analysis of the Mr 8600 fragment and comparison with the amino acid sequence derived from human C3 cDNA [de Bruijn, M. H. L. & Fey, G. H. (1985) Proc. Natl. Acad. Sci. USA 82, 708-712] placed it between residues 1199 and 1274 of the C3 sequence. Several peptides were synthesized according to the derived C3 sequence of amino acid residues 1209-1236. Based on their differential binding to CR2 and mAb 130, we localized the CR2-binding site and mAb 130 neoantigenic site, respectively, to residues 1227-1232 and 1217-1232 of the C3 sequence.

Amino Acid Sequence↗
PubMed1986

Cell cycle control of activated, synchronized murine B lymphocytes--roles of macrophages and complement C3.

Three restriction points control the cell cycle of activated murine B lymphocytes in a synergistic way. The first is controlled by the occupancy of surface immunoglobulin either by antigen- or by immunoglobulin-specific antibodies. The second is controlled by the complement C3d receptor CR2 which can be occupied by cross-linked C3b or C3d to stimulate the entry into S phase, or by soluble C3d or a C3 alpha-chain peptide, binding to the CR2 receptor, which inhibit the entry into S phase. Macrophages produce so-called alpha factors which also control the B-cell cycle at the same point. Thus, it is suspected that macrophages produce components of the early pathway of complement activation which finally lead to cross-linking of CR2 receptors on B cells. The third restriction point is controlled by unknown receptors that recognize so-called beta factors produced by helper T lymphocytes.

Animals↗
PubMed1985

Early- and late-phase activation of complement evaluated by plasma levels of C3d,g and the terminal complement complex.

Activation of the initial part (early phase) and terminal part (late phase) of the complement cascade was examined. C3d,g and the fluid-phase terminal complement complex were quantified and compared after spontaneous in vitro activation and after acute in vivo activation caused by extracorporeal circulation during coronary artery surgery. The results suggest that there is a close but not complete correlation between early- and late-phase activation of complement, that C3d,g and the terminal complement complex have different elimination rates in vivo, and that these two indicators are valuable for evaluation of early- and late-phase activation, respectively.

Complement Activation↗
PubMed1992

Loss of erythrocyte complement receptors (CR1; CD35) in patients with acute episodes of septicaemia or bacterial meningitis.

14 patients with septicaemia or bacterial meningitis were examined for serum levels of erythrocyte complement receptors CR1 (C3b/C4b; CD35) by an enzyme-linked immunosorbent assay and levels of circulating immune complexes (IC) by a polyethylene glycol precipitation complement consumption method, and concentrations of complement C3d split products in plasma by intermediate gel rocket immunoelectrophoresis. The CR1 receptor levels were significantly lower on day 7-8 after admission than on day 1-2 (p = 0.01), and than the levels 3-4 months later (p = 0.002). Both the levels of IC in serum and the C3d concentrations were significantly higher on day 7-8 than 3-4 months later (p = 0.02 and p = 0.004). The mechanism behind a temporary decreased expression of CR1 in patients with acute episodes of septicaemia or purulent meningitis is not fully known, and further investigations are needed to clarify whether this reduction in erythrocyte CR1 causes an impaired disposal of IC in patients with infections.

Acute Disease↗
PubMed1988

Autorosette inhibition factor: a positive acute phase reactant in interstitial cystitis.

Autorosette inhibition factor (AIF), complement C3d and eosinophil cationic protein (ECP) in urine were determined in 28 patients with painful bladder disease. In patients with interstitial cystitis (IC), diagnosed by the demonstration of detrusor mastocytosis, a positive correlation (r = 0.73, p less than 0.01) between AIF and C3d was found, whereas no reliable correlation was found in the remaining patients. The median concentration of urinary ECP was significantly elevated in the group of patients with IC whereas the median concentration of C3d was significantly elevated in both groups. AIF seems to behave as a positive acute phase reactant in IC. It is hypothesized that AIF may play a role in the pathogenesis of IC by influencing the normal barrier function of the epithelium of the bladder.

Acute-Phase Proteins↗
PubMed1985

Circulating immune complexes in myelofibrosis.

17 patients with idiopathic myelofibrosis were studied for the occurrence of circulating immune complexes (IC), using a polyethylene glycol complement consumption and a polyclonal rheumatoid factor inhibition assay. In 13 patients complement C3d was determined by rocket immunoelectrophoresis. Circulating IC were detected in 6 patients and were primarily found in patients with short duration of disease from time of diagnosis. The median duration of the disease in IC-positive patients was 4 months, compared to 12 months in the IC-negative group (P less than 0.05). 9 of the 13 patients investigated had increased levels of plasma C3d. However, there was no correlation to the occurrence of IC. It is concluded that circulating IC may take part in an immune-mediated bone marrow damage. This may involve deposition of IC in the bone marrow with secondary inflammation responsible for the development of bone marrow fibrosis.

Adult↗
PubMed1985

Amino acid sequence of the trypsin-generated C3d fragment from human complement factor C3.

Human C3d (try-C3d), prepared from trypsin-digested C3, was fragmented by cleavage with CNBr. Eight peptides were defined and separated by h.p.l.c. on reversed-phase columns. By automatic Edman degradation the complete sequences of five peptides and partial sequences of three peptides were determined. To obtain overlapping peptides the latter three fragments were digested with trypsin, chymotrypsin or Staphylococcus aureus V8 proteinase, after which the fragments were separated on reversed-phase columns. Two of the CNBr-cleavage peptides were completely sequenced, and 70% of the sequence of the remaining CNBr-cleavage peptide was determined. The non-sequenced part represents a very hydrophobic segment of try-C3d. The sequence data obtained represent 90% of the primary structure of try-C3d. Alignment of the CNBr-cleavage fragments was made easier by comparison with the cDNA sequence of mouse pro-C3 [Wetsel, Lundwall, Davidson, Gibson, Tack & Fey (1984) J. Biol. Chem. 259, 13857-13862]. Comparison of try-C3d with the equivalent part of human C4B revealed an extensive sequence homology in the N-terminal half of the molecules.

Amino Acid Sequence↗
PubMed1976

Complement receptors (C3b, C4b/C3d) unbalance on CLL lymphocytes.

A study of lymphocytes bearing C3b, C4b and C3d complement receptor (CRL) was performed on human peripheral blood from 16 healthy donors and 12 patients affected with Chronic Lymphatic Leukemia (CLL). In the latter group a clear rise of C3dCRL was demonstrated, when compared with immunoadherence receptors bearing lymphocytes. However, when compared with controls, also these latter were slightly augmented. Furthermore in CLL under treatment CRL populations showed the same profile as CLL: so it was suggested that the treatment reduced not selectively all the three types of CRL, within the population of sIg bearing lymphocytes. Here we discuss the hypothesis that, in CLL, the proliferating lymphocytes population is chiefly sIg+, C3d+/C3b-, C4b-, but also sIg+, C3d+/C3b+, C4b+.

Animals↗
PubMed1984

Circulating immune complexes and complement breakdown product C3d in glomerulonephritis and kidney transplantation.

Circulating immune complexes (CIC) and the complement breakdown product C3d were measured in 81 patients with glomerulonephritis (GN), 28 patients with early and 25 patients with long-term renal transplants. CIC were measured by a Clq-binding assay and C3d by a double-decker rocket immunoelectrophoresis. In patients with GN, CIC were detected in 19 and elevated C3d levels found in 45 patients. The highest levels of C3d were found in patients with membranoproliferative GN type I and II, diffuse sclerosing GN and GN secondary to SLE and Wegener's granulomatosis. No relationship was found between CIC and C3d, and the combination of CIC with C3d measurements did not help to characterize 'nephritogenic' CIC. C3d was frequently elevated in patients with impaired renal function which may reflect an inflammatory 'nephritic' process, but may also be due to a reduced renal elimination. Furthermore C3d was frequently elevated in patients with improving or decreasing renal function, and in patients with heavy proteinuria. Longitudinal studies of renal transplant patients suggested that immunosuppressive treatment decreased the C3d level. Patients with early renal transplants had elevated C3d levels that normalized during the first month after successful transplantation. CIC and elevated C3d were not related to onset of acute rejection episodes in early transplant patients nor to late renal graft failure.

Antigen-Antibody Complex↗
PubMed1991

The significance of complement in proliferative vitreoretinopathy.

Complement is the principal effector arm of antibody-mediated allergic response and plays a central role in the pathogenesis of many immunologic disorders. The possible pathophysiologic importance of complement was examined in the development of proliferative vitreoretinopathy (PVR). Vitreous aspirates from patients with idiopathic PVR (n = 21) and traumatic PVR (n = 15) were examined for total vitreal protein (TVP) and complement components C3, C3d, C4, and C1q-fixed immunoglobulins using enzyme-linked immunosorbent assay (ELISA), sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and western blotting. The TVP, C3 components, and factor C4 were elevated significantly in diseased vitreous. The C3-TVP and C4-TVP ratios showed no difference between traumatic and idiopathic PVR. A C4 index to estimate the rate of intraocular C4 synthesis had a mean value of 3.2 (n = 15). The increased relative amount of C3d reflected complement activation in diseased vitreous. The negative values in normal human serum and plasma and in patient plasma samples (n = 15) indicated a local reaction in the eye. The authors found C1q-fixed immunoglobulin G; this may be the cause of complement activation by the classic pathway. These findings support the opinion that the cause of PVR may be based partly on an autoimmune reaction against ocular structures.

Autoimmune Diseases↗
PubMed1983

Complement C3c and C3d in plasma and synovial fluid in rheumatoid arthritis.

By means of recently developed immunochemical assays increased levels of the complement C3c and C3d split products were found in synovial fluids of patients with rheumatoid arthritis (RA) as compared with synovial fluids of patients with traumatic synovitis (TS). In plasma, only the C3d levels were significantly increased compared with plasma levels of patients with TS. Both split products were higher in RA synovial fluids (SF) than in RA plasma. A positive correlation between the C3d concentrations in plasma and the presence of IC in serum was found, and between the C3c levels and the concentration of polymorphonuclear cells in SF of RA patients. Due to differences in turn-over of C3c and C3d determination of plasma C3d levels may be a useful parameter for the evaluation of immunological activity in RA, while measurement of C3c in the synovial fluid may elucidate the actual inflammatory activity in the synovial membranes.

Antigen-Antibody Complex↗
PubMed1987

Expression of CR1 and CR2 complement receptors following Epstein-Barr virus infection of Burkitt's lymphoma cell lines.

Epstein-Barr virus (EBV) infection of human B lymphocytes involves a specific receptor closely associated with, or identical to, the C3d complement receptor, CR2. Thus, 25 out of 29 EBV-positive Burkitt's lymphoma (BL) cell lines but none of 15 EBV-negative BL lines were found to express C3 receptors. Furthermore, in vitro infection with EBV of six EBV-negative cell lines resulted in the expression of C3 receptors in association with that of EBV-determined nuclear antigen (EBNA). Rosette assays using erythrocytes coated with human C3b, C3bi, and C3d, inhibition of rosette formation with anti-receptor antibodies, and flow cytometry analysis of stained cells demonstrated that EBV-converted lines expressed C3b and C3d receptors, CR1 and CR2. Anti-receptor antibodies recognized an average of 40,700 anti-CR1 and 140,000 anti-CR2 binding sites on an EBV-converted line (BL41/B95), whereas no specific binding occurred on the corresponding EBV-negative (BL41) cells. Because CR1 and CR2 are involved in B-cell proliferation and/or differentiation, enhanced expression of C3 receptors following the interaction between EBV and B cells and/or subsequent infection of the cells by EBV may provide a basis for positive control of B lymphocyte proliferation by EBV.

B-Lymphocytes↗
PubMed1987

Molecular cloning of the cDNA encoding the Epstein-Barr virus/C3d receptor (complement receptor type 2) of human B lymphocytes.

Complementary DNA clones for complement receptor type 2 (CR2), the B-lymphocyte membrane protein that serves as the receptor for Epstein-Barr virus and the C3d complement fragment, were obtained by screening a lambda gt11 library generated from Raji B lymphoblastoid cell mRNA. A 4.2-kilobase (kb) clone, representing the entire coding sequence of the protein plus untranslated 5' and 3' nucleotide sequences was obtained and sequenced. The 4.2-kb clone, which contains all but about 500 base pairs (bp) of the 5' untranslated region of the full-length CR2 mRNA, consists of 63 bp of 5' untranslated nucleotide sequence followed successively by a start codon, a 20-amino acid hydrophobic signal peptide, 1005 amino acids having a repeating motif, a 28-amino acid probable transmembrane domain, and a 34-amino acid cytoplasmic tail. The deduced amino acid sequence of the protein indicates that the extracellular domain consists entirely of 16 tandemly arranged repeating elements, each 60-75 amino acids in length, which are identified by multiple conserved residues. This repeating motif also occurs in the C3b/C4b receptor, several complement proteins, and a number of noncomplement proteins. In CR2, the 16 repeats occur in four clusters of four repeats each. Approximately 10% of the deduced amino acid sequence, including the amino and carboxyl termini, was confirmed by amino acid sequencing of tryptic peptides derived from purified CR2. The nucleotide and derived amino acid sequence of CR2 and related studies are presented here.

Amino Acid Sequence↗