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PubMed1993

C3d levels in normal individuals of Chinese origin.

The level of C3d in the urine and serum of normal healthy Chinese individuals was determined by enzyme-linked immunoassay. Urine levels were found to be in the range of 0.1-2.3 ng/mmol/l creatinine (n = 87, mean = 0.242 microgram /ml). Serum levels were in the range of 10.1-37.6 micrograms/ml (n = 30, mean = 22.6 micrograms/ml). C3d clearance was also determined in 10 selected normal healthy individuals with random urine levels in the upper, middle and lower range. Results suggest that there may be individual variability in the way in which C3d is cleared from blood in normal individuals and it is suggested that caution is necessary in interpreting single urine C3d estimations.

Asian People↗
PubMed1978

Complement receptor subtypes C3b and C3d in lymphatic tissue and follicular lymphoma.

To substantiate the origin of follicular (nodular) lymphoma cells from germinal-centre cells, the lymphoma cells from 7 patients with follicular lymphoma and from 9 tonsils and 2 lymph nodes were studied for the presence and distribution of complement-receptor subtypes (i.e., the receptors for C3b and C3d). It was found that erythrocytes coated with antibodies and C3d (EAC3d) adhered exclusively to germinal centres, whereas erythrocytes coated with antibodies and C3b (EAC3b) adhered to germinal centres and in many instances to the regions between them. These findings indicate that germinal-centre cells bear both complement-receptor subtypes and that the B cells of the interfollicular area, which belong at least in part to the precursors of plasma cells, bear only a receptor for C3b. In frozen sections of follicular lymphomas, a similar distribution of complement-receptor subtypes was observed; EAC3d was bound exclusively to the neoplastic nodules, and EAC3b adhered to the neoplastic nodules and adjacent paranodular tissue. Receptor studies on suspended cells of both normal tonsils and follicular lymphomas revealed a slight predominance of EAC3d(+) cells or equal numbers of EAC3b(+) and EAC3d(+) cells. The complete congruence in the expression and distribution of complement-receptor subtypes between tissues from follicular lymphomas and those from normal and hyperplastic tonsils or lymph nodes suggests that follicular lymphoma represents the neoplastic counterpart of the reactive germinal centre.

Binding Sites↗
PubMed1990

Epstein-Barr virus (EBV) receptors on epithelial hybrid cells derived from nasopharyngeal carcinoma.

We previously established an Epstein-Barr virus (EBV) genome-positive epithelial hybrid cell line, designated NPC-KT, which was prepared by fusing primary epithelial cells derived from nasopharyngeal carcinoma (NPC) with an epithelial Ad-AH cell line. In this study, we measured the presence of the EBV receptors using radiolabelled EBV. It was determined that similar amounts of Burkitt's lymphoma (BL)-derived P3HR-1 or NPC-KT-derived EBV can attach BL-derived Raji cells, but that only P3HR-1 virus can attach to NPC-KT cells. In addition, the superinfection of NPC-KT cells with P3HR-1 virus could not be inhibited by pretreatment with a monoclonal antibody against C3d (OKB7). Raji cells adsorbed with OKB7 became much less susceptible to superinfection with P3HR-1 or NPC virus. The data suggest that EBV receptors unrelated to C3d receptor exist.

Cell Line↗
PubMed1985

Steroids reduce complement activation in rheumatoid arthritis.

Patients with seropositive, classical rheumatoid arthritis (RA) with severe active disease have raised plasma concentrations of the complement C3 split product C3d. These values display little diurnal or circadian variation in the individual patient. During a 3-month period the variation was within 10 mU/l in 45 patients (ref. range 20-52 mU/l, RA patients up to 120 mU/l.) Six RA patients were treated with steroids on clinical indication, and the plasma C3d, Ritchie index and pain score before and during the treatment (30 mg prednisolone per day) were measured. The variables showed a steady decrease during the next 14 days. Plasma C3d fell 2/3 of the total fall within the first 48 hours, while the serum total haemolytic complement activity, complement C3 and C4 did not change significantly. This shows that the anti-inflammatory effect of steroids is accompanied by a reduction of complement activation.

Arthritis, Rheumatoid↗
PubMed1989

The Epstein-Barr virus receptor on two nasopharyngeal carcinoma model cell lines.

It was reported that the OKB7 monoclonal antibody to C3d receptor could directly inhibit Epstein-Barr virus (EBV) attachment to and infection of B-lymphocytes. So we tested whether the OKB7 could inhibit superinfection of two epithelial NPC model cell lines (D98/HR-1 and NPC-KT) with EBV. Pretreatment of B-lymphocytes with the OKB7 significantly inhibits EBV infection. However, pretreatment with the OKB7 had no effect on superinfection of D98/HR-1 and NPC-KT cells. These data suggest that an EBV receptor, unrelated to C3d receptor, exists.

Antibodies, Monoclonal↗
PubMed1990

CR2 complement receptor.

CR2, a membrane glycoprotein, is one of a number of cell-surface proteins which bind activation and processing fragments of the complement system. CR2, which is found on normal B lymphocytes, follicular dendritic cells in lymphoid organs, and epithelial cells, interacts preferentially with C3dg, the terminal activation/processing fragment of the third complement component. Attachment of C3dg to CR2 brings complement activators, bearing covalently bound C3dg, into direct membrane contact with CR2-bearing cells. Epstein-Barr virus, a human herpesvirus, also binds to CR2 on B lymphocytes. Attachment of EBV is followed by infection. CR2 has been purified and the binding properties of its ligands analyzed. Monoclonal antibodies have been developed and used to probe the structural correlates of CR2 functions. CR2 has been molecularly cloned and its primary amino acid sequence deduced. These data indicate that it shares characteristic structural features with a number of other complement and non-complement cell membrane and plasma proteins. Several of the complement-associated proteins in this family possess regulatory functions; they are encoded by linked genes which have been localized to band q32 on chromosome 1. CR2 has been expressed in primate and rodent cells by transfection of cDNA in antigenically and functionally intact form. It has also been expressed in soluble form and its structure, electron microscopic appearance and binding characteristics analyzed in detail. The present state of knowledge of the structure and genetics of CR2 and current understanding of its biologic functions are summarized here.

Animals↗
PubMed1985

Generation of C3d,g and C3d by urokinase-treated plasma in association with fibrinolysis.

In the breakdown of fluid phase C3 in plasma, the process of conversion of iC3b to C3c and 'C3d' has not been elucidated. Using fluorescent labeled iC3b as a substrate, urokinase (UK) treated but not normal plasma was found to exhibit effective 'C3d' production. To address the relationship between the fibrinolytic activity specific for UK-activated plasma and this 'C3d' production, an assay system was developed that permitted the simultaneous determination of both activities. This method indicated that 'C3d' generation paralleled that of plasmin-dependent fibrinogen degradation. A Km of iC3b for plasmin was 3.0 X 10(-6) mol/l which is similar to the Km of fibrinogen. Plasmin cleavage of iC3b gave rise to C3d1 (Mr 42,000) and C3d2 (Mr 28,000). Purified plasmin C3d1 showed the same Mr and pI as C3d,g prepared from iC3b, by H and I. C3d2 was derived from C3d1. From these in vitro experiments with urokinase-treated plasma, we conclude that in parallel with fibrinolysis efficient cleavage of fluid phase iC3b to C3c + C3d,g and C3d occurs and we hypothesize that this is one mechanism for the generation of C3d in vivo.

Complement C3↗
PubMed1985

Mixed-pattern immune deposit glomerulonephritis in a child with inherited deficiency of the third component of complement.

The renal histopathology of a 7-year-old Laotian male with inherited deficiency of the third component of complement, recurrent infections, and persistent hematuria and proteinuria is described. The histologic changes are predominantly those of mesangiopathic disease with isolated changes resembling type I membranoproliferative glomerulonephritis and transmembranous glomerulonephritis. IgG, IgA, IgM, C4, and fibrinogen, but not C3, were detected by immunofluorescence in mesangial zones and in segments of capillary walls. A normal distribution of C3b receptors was present along all capillary walls. This report provides additional support for the association of congenital C3 deficiency and immune deposit glomerulonephritis.

Child↗
PubMed1985

Adult respiratory distress-like syndrome during hemodialysis: relationship between activation of complement, leukopenia, and release of granulocyte elastase.

Twelve patients with terminal uremia (8 females and 4 males) treated with chronic maintenance hemodialysis, were extensively studied during two successive dialyses with alternate use of either a Cuprophan (CP) based membrane, or a Polycarbonate (PC) membrane. Arterial plasma levels of total hemolytic complement, complement factors C3d and C5a, and granulocyte derived elastase were determined immediately before dialysis and sequentially during the entire procedure. Effluent line from the hemodialyzer was similarly sampled. Collected samples were centrifuged immediately at the bedside and instantly frozen in liquid nitrogen in order to preserve labile plasma components of complement. Analysis of the overall results shows that initial arterial leukopenia and generation of C5a in the hemodialyzer, as well as maximal values of hemodialysis-induced free plasma C3d and granulocyte elastase are related. Reflecting differences in biocompatibility, CP membranes were shown to induce significantly more leukopenia, increase in plasma free C3d, generation of C5a, and release of granulocyte-derived elastase. These results indicate that activation of complement, leukopenia, and release of granulocyte derived elastase are interlinked pathophysiological mechanisms of importance for acute deterioration of pulmonary function during hemodialysis, and that this condition is closely related to adult respiratory distress syndrome (ARDS).

Adult↗
PubMed1983

Use of monoclonal anti-C3 antibodies to characterise the fragments of C3 that are found on erythrocytes.

Using monoclonal antibodies to C3 it has been shown that the red blood cells of patients with cold haemagglutinin disease carry on their cells C3d,g (alpha-2D-globulin) rather than C3d. C3d,g seems to be the final product of in vivo C3 activation in fluid phase and on red cells. The cleavage of C3dg to C3d and C3g does not appear to occur in vivo either in the fluid phase or on red cell bound C3bi. In vitro C3-coated red cells prepared by antibody or low ionic strength techniques produce cells with C3d and C3bi as the predominant C3 fragment, whereas the Fruitstone technique in which coating occurs by the alternative pathway has principally C3b. The activity of C3 cleaving enzymes in whole serum is strongly influenced by the ionic conditions of the serum.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

Synergy test for recognition of epitopes on soluble proteins; its application in the study of CD21 and CD23 antigens and their respective antibodies.

Antigens such as CD21 and CD23, which express only one copy of an epitope require two monoclonal antibodies (mAbs) for their detection and estimation. This requirement is exploited in two ways in a technique based on the chromic chloride haemagglutination test. For simple titration of antigen two portions of red cells each coated with one of a pair of synergising mAbs are used in a 1:1 combination. For testing the antigenic specificity of a mAb and assessing its region of epitope binding, the mAb under test is serially diluted in fluid containing a standard amount of antigen and red cells are added to which have been attached a different mAb. If the red cell-bound mAb recognises a determinant topographically distinct from that of the soluble mAb, red cell agglutination to high titre occurs. In titrations of ascitic fluid containing approximately 1 mg/ml mAb, titres of log2(9) to log2(16) were recorded from a starting dilution of 1 in 200. Hence the test is very sensitive and only minute amounts of a mAb are required for testing. The same test system can be used for assessing the relative display of epitopes on antigen obtained from different sources, e.g., culture supernates and body fluids. The method is of general applicability to monomeric antigens and its use is illustrated by analysis of CD21 and CD23 antigens and antibodies.

Animals↗
PubMed1991

Identification of 5'-regions affecting the expression of the human CR2 gene.

Human CR2 has a restricted cellular distribution, being expressed on B lymphocytes, dendritic cells of the spleen, pharyngeal epithelial cells, and at low levels on some T lymphocytes. CR2 is expressed by mature B lymphocytes, but not by pre-B cells or by plasma cells, suggesting that mechanisms exist for positive and negative regulation of CR2 gene expression during B cell development. S1 nuclease digestion and primer extension analysis positioned the transcriptional start site between 92 and 94 bp upstream of the ATG codon. Nucleotide sequence analysis identified several sequences within the CR2 promoter region with homology to other known promoter sequences. These included a site similar to an AP-1 site, a sequence with 10 of 13 nucleotides identical to the X box of class II genes, and a TATA box. Genomic DNA starting immediately 5' of the sequence encoding the CR2 signal peptide was subcloned upstream of the bacterial chloramphenicol acetyltransferase gene for analysis of functional promoter and enhancer sites. The functional boundaries of the CR2 promoter were determined by deletion analysis, with both the X box-like sequences and the TATA box required for CR2 expression. This analysis revealed sequences with regulatory effects on CR2 gene expression, however, these transcriptional controlling sequences did not act in a tissue specific fashion.

Antigens, Differentiation, B-Lymphocyte↗