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PubMed1992

Expression of the C3d-binding protein (CR2) from Candida albicans during experimental candidiasis as measured by lymphoblastogenesis.

The complement C3d-binding protein (CR2) of Candida albicans has been purified by immunoaffinity chromatography, and its specificity has been characterized by immunoblotting with monoclonal antibodies to the C. albicans CR2 and the mammalian CR2. Recent studies with immunoelectron microscopy indicated that the CR2 was expressed during a systemic infection in a murine model of candidiasis. As a continuation of these observations, the immunogenicity of the C. albicans CR2 was investigated in a lymphoblastogenesis assay. Lymph node cells as well as splenic lymphocytes from mice infected subcutaneously with viable blastoconidia of C. albicans reacted to the C. albicans CR2 to a significantly greater extent than did lymphocytes from uninfected mice (P less than 0.01). The maximum stimulation of splenic lymphocytes by the purified receptor occurred at a concentration of 0.54 micrograms of protein per ml after 72 h of incubation of lymphocytes and receptor. Also, splenocytes from infected or CR2-immunized mice exhibited significantly reduced responses to the T-cell-dependent mitogen phytohemagglutinin (P less than 0.01). These data indicate that lymphocytes from infected mice respond to the C. albicans CR2 in a lymphoproliferation assay to a greater extent than do lymphocytes from uninfected mice, indicating that the CR2 is expressed in vivo.

Animals↗
PubMed1984

A simple method for quantitative measurement of C3d in human plasma.

We describe a simple and reliable method for quantitating C3d in human plasma. The method rests on the finding that native C3 and its activation/inactivation product C3c bind to Concanavalin A, whereas C3d does not. Rocket affinoimmunoelectrophoresis with Con-A Sepharose incorporated into an intermediate gel permits quantitation of free C3d in 2-20 microliters aliquots of EDTA-plasma without any manipulation prior to sample application. Using this method, we found that the level of circulating C3d in plasma of 30 healthy donors was usually well below 3% of maximally convertable C3d.

Complement C3↗
PubMed1975

Immunologic cell features in lymphocytic leukemias: a review.

Since four years, it has been possible to classify most cases of Chronic Lymphocytic Leukemia (CLL) as given to the expansion of abnormal B-lymphocytes. On the contrary, the T-cell class is apparently normal and the T cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value. The clonal nature theory of B-lymphocytes in CLL is substantiated by the fact that, in general, in every patient only one Ig light chain determinant is present. Again, when serum Ig monoclonality is present in CLL, it appears idiotypically identical to the Ig shown by the lymphocytes of the same patient. Among the most important B-lymphocyte abnormalities in CLL, there are: (a) fluorescence of surface Ig is usually less intense than that in normal subjects, and fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20 folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement (C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. All the above-mentioned data, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency.

Animals↗
PubMed1975

Lymphocyte immunological patterns in leukaemia: a review.

Investigation of the cell S--Ig in acute lymphocytic leukaemia (ALL), at the onset of relapse of the disease, shows quite marked differences from patient to patient according to the extent of the immunofluorescent-positive cells. They may vary from 0.5 to 25% or more. When these Ig-positive cells are treated with trypsin and then incubated "in vitro" for six hours, many of them are no longer Ig-positive, i.e. they do not synthesize Ig. It might be possible, that the membrane-Ig observed before trypsinization does not represent true Ig-determinants of mature B-cells (antibodies attached to leukaemia-specific determinants?). The extent of these features decrease in remission until their disappearance. Relationship between the cell immunological patterns and the treatment response in ALL could exist. In a group of ALL-patients under the same treatment, that is, vincristine and prednisone, the correlation between the course of the disease after the above-mentioned therapy showed quick and complete remission in patients with low percentage of Ig-positive cells (below 10%) and poor improvement (often without complete remission) in patients with higher percentage of Ig-positive cells. Among the most important B-lymphocyte abnormalities in chronic lymphocytic leukaemia (CLL) are the following: (a) fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20-folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. Results of the observations on lymphocytes in CLL, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency. On the contrary, the T-cells class is apparently normal, and the T-cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value.

B-Lymphocytes↗
PubMed1983

Platelet-associated complement C3 in thrombocytopenic states.

Platelet-associated complement components C3, C3d and C4 (PAC3, PAC3d, PAC4) were quantitated by a modification of the platelet radioactive anti-IgG test using highly purified C3 antibodies in 74 patients with immune thrombocytopenia (ITP), 26 patients with presumed nonimmune thrombocytopenia (NTP), and 114 normal individuals. Elevated PAC3 levels were found in 26 out of 74 patients with ITP (35%) and in 10 out of 26 patients with NTP. Although the percentage of elevated PAC3 values was higher in thrombocytopenic patients than in nonthrombocytopenic patients, no statistically significant correlation existed between platelet counts and PAC3 levels, neither for ITP nor for NTP. However, such a relationship was demonstrable between PAC3 and platelet-associated IgG, both for ITP (P less than 0.05) as well as NTP patients (P less than 0.001). We conclude that elevated PAC3 values are not restricted to immune thrombocytopenias. Quantitative differences of PAC3 between ITP and NTP patients suggest that part of the PAC3 is immunologically mediated and has a role in the pathogenesis of autoimmune thrombocytopenias.

Adult↗
PubMedDate not supplied

Biochemical pathways of acute lung injury.

Complement fragments (C3, C3d, C5a), thromboxane B2 (TxB2), 6-keto-PGF1 alpha and immunoreactive trypsin (IRT) were measured in 98 patients at risk of developing the adult respiratory distress syndrome (ARDS): 53 multiple trauma, 28 abdominal surgery and 17 acute pancreatitis. Sixty-five of these patients developed ARDS: 30 multiple trauma, 19 abdominal surgery and 16 acute pancreatitis patients. Forty of the 65 ARDS patients and 9 out of the 33 non-ARDS patients died. Mean value of the C3d to C3 ratio was abnormal in both ARDS and non-ARDS patients. C5a-like activity was detected in 70 out of the 98 patients (49 ARDS and 22 non-ARDS patients). TxB2 abnormal values (greater than 100 pg . ml-1) were found in 70% of the patients, especially when sepsis occurred. No correlation could be made between abnormal 6-keto PGF1 alpha values and ARDS or sepsis. The mean peak IRT value was 675 micrograms . 1(-1) for ARDS patients and 274 micrograms . 1(-1) for non-ARDS patients (p less than 0.05). A firm correlation was also measured between IRT and sepsis (p less than 0.01). C5a-like activity was regularly detected soon after injury, while TxB2 and IRT tend to appear later in patients developing ARDS. Neither C3d/C3, nor C5a-like activity, nor TxB2, nor IRT are specific markers of ARDS, since they also appeared in severely ill patients who did not develop ARDS.

6-Ketoprostaglandin F1 alpha↗
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↗
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↗
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↗