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PubMed1990

Purification and characterization of the extracellular C3d-binding protein of Candida albicans.

A C3d-binding glycoprotein was purified from the culture filtrate of Candida albicans by preparative isoelectric focusing. The protein possessed a pI of 3.9 to 4.1 and could inhibit rosetting of EAC3d (sheep erythrocytes conjugated to C3d) by pseudohyphae of C. albicans. When analyzed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and mercaptoethanol, the protein migrated as a doublet with apparent molecular masses of 55 and 60 kilodaltons (kDa) and as a 50-kDa band in nonreducing gels. These results were observed with Aurodye stain for proteins. Western immunoblot, and concanavalin A stain, which indicates that both bands contain carbohydrate as well as antigenic determinants. The treatment of purified glycoprotein with endoglycosidase F but not endoglycosidases H, N, and O resulted in a complete conversion of the doublet into a faster-migrating broad band with an apparent molecular mass of 45 kDa. When the amino acid analysis of the C3d-binding protein was compared with that of the CR2 from B lymphocytes, significant differences were observed. These data indicate that C. albicans secretes a C3d-binding protein during growth in vitro which appears to be different from the mammalian C3d receptor.

Amino Acids↗
PubMed1990

Glomerular CR1 express in situ cofactor activity for degradation of C3b.

Adherence of sheep erythrocytes (E) sensitized with IgM antibodies (A) and C3b (EAC3b) to C3b/C4b receptors (CR1) in cryostat sections of human renal glomeruli was studied using the closed chamber technique. The adsorption was stable for at least 3 h at 37 degrees C. In the presence of purified factor I, the indicator cells, however, detached from the sections after 30 min at 37 degrees C. Factor H was not required. The release was not due to loss of CR1 activity in the tissue. The detached indicator cells were negative in the immune adherence test and were agglutinated by antibody to C3d, but not by antibody to C3c. Western blot of the detached indicator cells revealed the presence of C3d and C3c was found in the chamber fluid. Accordingly, detachment of the indicator cells was due to degradation of C3b to C3d with the release of C3c into the chamber fluid. Protease inhibitors did not prevent the detachment of the indicator cells. EAC3b incubated with sections of renal glomeruli preincubated with anti-CR1 antibody were not degraded. The results therefore indicate that CR1 in situ in renal glomeruli can provide the necessary cofactor activity for factor I-mediated degradation of C3b to C3d and C3c.

Complement C3b↗
PubMed1990

Reduction of complement activation in rheumatoid arthritis by steroid treatment.

Patients with severe active active rheumatoid arthritis (RA) have higher than normal plasma concentrations of the complement C3 split-product C3d, indicating increased complement activation. Treatment with steroids reduced plasma C3d levels in these patients. Ten patients with classic or definite RA and high disease activity were studied during six days of treatment with steroids. The C3d plasma concentrations declined in a dose-related manner with an increase in daily prednisolone dosage. However the statistical significance of this relationship did not seem to be high enough to validate the use of serial C3d estimations to monitor changes in disease activity in RA patients during short-term steroid treatment.

Arthritis, Rheumatoid↗
PubMed1993

Deposition of C3, the terminal complement complex and vitronectin in primary biliary cirrhosis and primary sclerosing cholangitis.

Characteristics of primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are bile duct destruction and portal inflammation. Increased levels of circulating complement activation products are also present. This raises the possibility of involvement of complement-dependent cytotoxic mechanisms in the pathogenesis. Therefore, we investigated liver biopsy specimens from 21 patients with PBC, six patients with PSC and six controls for complement deposits by immunohistochemistry using polyclonal and monoclonal antibodies against C3d, the terminal complement complex (TCC) and vitronectin (S-protein). We found C3d, TCC and vitronectin deposits only in the portal tracts. C3d and TCC were present in the walls of the hepatic arteries and in the connective tissue stroma but never around the bile ducts. We found vitronectin deposits throughout the connective tissue, often independent of the TCC deposits. When vitronectin and TCC were co-localized, the staining patterns were inverse; that is, intense staining for TCC accompanied weak staining for vitronectin and vice versa. Occasionally complete dissociation between TCC and vitronectin staining was observed. Deposits of TCC and vitronectin showed a focal distribution leaving many portal tracts free of TCC. Our results question whether complement-dependent cytotoxic mechanisms take part in the bile duct destruction in PBC and PSC.

Adult↗
PubMed1998

Antisulfatide polyneuropathy: antibody-mediated complement attack on peripheral myelin.

Increased titers of circulating antisulfatide antibodies are consistently associated with a variety of chronic axonal and demyelinating polyneuropathy syndromes. Previous studies have shown that the pattern of antisulfatide binding to neural tissues correlates with the type of neuropathy. This suggests a possible role for antisulfatide antibodies in inducing peripheral nerve dysfunction, although their exact contribution to the pathogenesis of neuropathy is still unknown. We examined sural nerve biopsy specimens from two patients with sensorimotor and small fiber sensory neuropathy associated with high titers of IgM monoclonal antibodies to sulfatide. Electrophysiological and pathological findings were consistent with predominant demyelination in the patient with sensorimotor involvement, whereas evidence of demyelination was obtained only by teased fiber examination in the other patient. The ultrastructural study disclosed in both cases the presence of myelinated fibers with widely spaced myelin, due to a separation of leaflets of the intraperiod lines. Immunocytochemistry, performed on frozen sections, demonstrated the presence of IgM and complement product C3d bound to myelin sheaths of almost all fibers. Few fibers were immunoreactive for complement components C1q and C5. In addition, the terminal complement complex neoantigen C5b-C9, not associated with S protein, was detected on some myelinated fibers. The results suggest that, at the least in some forms of demyelinating neuropathy associated with antisulfatide antibodies, pathological changes are complement mediated. Our data further confirm previous clinical and experimental observations that complement activation initiates separation of myelin intraperiod lines.

Aged↗
PubMed1985

The quantitation of C3d by routine methods after the direct absorption of human plasma with anti-C3c.

The immunological methods for quantitating C3d in plasma require first the removal of less fragmented intermediates as well as the intact C3. We describe an alternative method for the quantitation of C3d in human plasma. The components which should be removed are absorbed (precipitated) directly in the plasma by a specific anti-C3c antiserum. It is then possible to determine the concentration of C3d by routine immunological methods.

Antibodies↗
PubMed1996

Activation of the complement cascade and increase of clusterin in the brain following a cortical contusion in the adult rat.

The aim of the present study was to examine the glial cell response and the possible involvement of the complement cascade following a cerebral cortical contusion. The lesion was produced using a standardized weight-drop technique in adult rats. The blood-brain barrier was damaged, as demonstrated by a decrease of immunoreactivity for a tight junction protein normally expressed by endothelial cells of small vessels in the central nervous system. Increased immunoreactivity for microglial (OX42) and astroglial cells (glial fibrillary acidic protein), as well as macrophages expressing ED1-immunoreactivity (IR) were found in the vicinity of the lesion at all postoperative survival times (2-14 days). In the present study complement factor C3d- and C9-IR was found around the lesion, indicating that activation of the complement cascade had taken place. Furthermore, immunoreactivity for the putative complement inhibitor clusterin (sulfated glycoprotein-2) was found in some of the injured neurons. The contralateral hemisphere showed no evidence of the reaction found in the ipsilateral hemisphere. The balance between complement activation and complement inhibitors may have an impact on the degenerative components in the brain following traumatic injury and in particular on the events leading to nerve cell death.

Animals↗
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↗