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PubMed1988

Expression of CR2/EBV receptors on human thymocytes detected by monoclonal antibodies.

The biologic effects of the third component of complement, C3, are mediated via receptors which specifically bind the enzymatic degradation products resulting from the cleavage of C3. One of the products, C3d, has been associated with binding to the second complement receptor CR2 (CD21). This receptor, which is identical to the receptor for Epstein-Barr virus (EBV), has been primarily found on cells of the B lineage, but not on mature T cells or other cells of erythroid or myeloid lineages. In the present investigation, we report the presence of CR2 on human thymocytes. Indirect immunofluorescence analysis employing monoclonal anti-CR2 antibodies revealed a range of thymocyte reactivity from 15% to 63% in thirteen experiments using cells of different donors. Reactivity was always greater with the monoclonal anti-CR2 (CD21) antibody HB-5 than with two other antibodies which recognize distinct epitopes on the CR2 molecule. Two-color immunofluorescence analysis indicated that the brightest of the HB-5-stained thymocytes also reacted with the monoclonal anti-CD1 antibody T6 (immature thymocyte marker) while some of the duller HB-5-staining cells reacted with the monoclonal anti-CD3 antibody Leu-4 (mature thymocyte marker). Immunoprecipitation of CR2 on thymocytes with antibody HB-5 and polyacrylamide gel electrophoretic analysis revealed a protein of 145 kDa molecular mass which is consistent with the size of CR2 found on B lymphocytes. These findings raise several questions regarding the biologic role of CR2-EBV receptor on cells of the T lineage.

Antibodies, Monoclonal↗
PubMed1978

Demonstration of immunoglobulin production by tumor cells in non-Hodgkin's and Hodgkin's malignant lymphomas and its significance for their classification.

Combined application of morphologic, immunochemical, and immunologic methods has led to a reinterpretation of non-Hodgkin's lymphomas and to the establishment of the Kiel classification. In the present paper, the main Ig-producing entities are considered. These are: 1. Chronic lymphocytic leukemia of the B-type (B-CLL)--a proliferation of lymphocytes and a few so-called prolymphocytes and lymphoblasts. The mean tissue IgM value is slightly increased; the serum IgM level is normal or reduced. The tumor cells bear SIg, and a majority of them have a receptor for C3d but always lack CIg and are usually devoid of receptors for C3b. 2. Lymphoplasmacytoid immunocytoma--a mixed proliferation of lymphocytes and centrocytes, blast cells, plasma cells, or plasmacytoid cells. The tissue Ig content is most often (91%) and most highly increased in this group, whereas the serum Ig level is increased in only 20% of the cases. The tissue IgM of 17 cases was shown to be monoclonal by IEF. Most tumor cells have SIg and a variable numbear CIg. The tumor cells bear both complement receptor subtypes, only a receptor for C3b, or no complement receptors at all. 3. Centroblastic/centrocytic lymphoma--usually a follicular proliferation of abundant small germinal center cells (centrocytes) and some large germinal center cells (centroblasts). The tumor cells bear SIg and both complement receptor subtypes. The C3b- and C3d-positive cells are located in the follicles, as in nonneoplastic lymphatic tissue. 4. Centrocytic lymphoma--a purebred, diffuse proliferation of the small germinal center cells (centrocytes). These cells bear SIg and receptors for C3b and C3d but usually lack CIg. 5. Centroblastic lymphoma--a proliferation of the large germinal center cells (centroblasts). 6. Lymphoblastic lymphoma of Burkitt's type. 7. Immunoblastic lymphoma--a diffuse proliferation of large basophillic cells resembling immunoblasts. The tissue IgM content is increased in 60% of the cases. It proved to be monoclonal with IEF in all five cases studied. The cells of five cases with increased tissue Ig content bore SIg. Nearly half of the cases studied showed CIg. Besides non-Hodgkin's lymphomas, paraffin sections of 87 biopsies from Hodgkin's disease were investigated for CIg in Hodgkin's and Sternberg-Reed cells. These cells stained positively in 68 cases, most often for IgG, followed by IgD. In five cases of the lymphocyte-depleted type, the staining of the Hodgkin's and Sternberg-Reed cells was restricted to one light chain type.

Burkitt Lymphoma↗
PubMed2002

Complement activation in infective endocarditis: correlation with extracardiac manifestations and prognosis.

In an infectious process complement activation is necessary for a proper immune and inflammatory response, but when exacerbated may cause tissue injuries. In infective endocarditis (IE) patients tend to develop high titres of circulating immune complexes (CIC) that activate complement. The aim of this study was to evaluate for the first time complement activation in IE for possible correlation with extracardiac manifestations and clinical prognosis. Twenty patients with IE, 14 healthy controls and 15 patients presenting mitral and aortic valve lesions (with no signs of either infection or other associated diseases), were studied. Plasma levels of C3adesArg, SC5b-9, C1rs-C1Inh and C3b(Bb)P were determined by ELISA and C3d by double decker immunoelectrophoresis. C3 and C4 levels were assayed by turbidimetry and CIC by ELISA. Elevation of plasma levels of all complement activation products, with the exception of C3b(Bb)P, indicated a significant classical pathway activation in IE patients when compared to controls (C3d: P < 0.00004; C3adesArg: P < 0.03, SC5b-9: P < 0.01, C1rs-C1Inh: P < 0.00007). CIC levels were significantly increased (P < 0.005) and C3 reduced in IE patients (P < 0.05). Elevated C3d (P < 0.02) and C3adesArg (P < 0.03) levels were associated with pulmonary manifestations. In addition, C3d was significantly elevated in the patients who died when compared to those who had a good recovery (P < 0.02). Our data demonstrate the activation of the complement classical pathway, most probably mediated by CIC, in IE and suggests C3d and C3adesArg as possible markers for extracardiac lesion and severity of the disease.

Adolescent↗
PubMed1988

Epstein-Barr virus (EBV) infection of murine L cells expressing recombinant human EBV/C3d receptor.

The normal host range of Epstein-Barr virus (EBV) is limited to primate B lymphocytes and certain epithelial cells that express the C3d/EBV receptor [complement receptor 2 (CR2, CD21)]. In the present study, expansion of the tissue tropism of EBV has been accomplished by stably transfecting the murine fibroblast L cell line with pMT.CR2. neo.1, a eukaryotic expression vector promoting the transcription of a complementary DNA insert encoding human CR2. High CR2-expressing transfected L cells were selected by fluorescence-activated cell sorting. The recombinant CR2 was shown to have the same molecular weight as wild-type CR2 from Raji cells and to mediate the binding by the transfectants of particles bearing the iC3b and C3d fragments of the third component of complement. All CR2-expressing L cells, but not nontransfected controls, also bound EBV, as assessed by indirect immunofluorescence. After a 60-hr culture, approximately 0.5% of the CR2-expressing cells preincubated with EBV demonstrated immunofluorescent staining of EBV nuclear antigen with serum from a patient with nasopharyngeal carcinoma. No fluorescent staining of cells was seen with monoclonal antibodies to the early antigen complex or to gp350/220, indicating that the infection was predominantly latent. Infected cells cultured for up to 4 weeks remained EBV nuclear antigen-positive. The capacity of recombinant human CR2 to confer on murine L cells susceptibility to stable latent infection by EBV indicates that this receptor is a primary determinant of the tissue tropism of EBV and may facilitate studies of cell-specific factors that regulate the viral growth cycle.

Animals↗
PubMed1978

Complement components in blood serum and suction blister fluid in erythropoietic protoporphyria.

Complement factor's C3c, C4, factor B, C3d and the immunoglobulin IgA were determined in suction blister fluid of patients with erythropoietic protoporphyria and in normal controls. The levels increased when the skin of the patients had been previously irradiated with 'white light', but with Kromayer radiation, and were interpreted as being the result of increased vasopermeability.

Adult↗
PubMed2001

Electrical current leakage during hemodialysis may increase blood-membrane interaction.

UNLABELLED: During hemodialysis blood - membrane interaction causes complement activation. During dialysis there may be an electrical current leakage to the dialyzer, especially if there is a broken ground or a defect in another electrical device coupled to the patient. This study investigated whether an electric current of 1.5 mA DC could alter blood membrane interaction as measured by changes in C3d in the blood. Such a high current leakage could occur because there is no protection in the dialysis machine (Class 1B) against auxiliary current leakage. Such a current could come from a defective external device in contact with the patient during hemodialysis. MATERIALS: A dialysis machine (Fresenius 2008C) with a filled blood-line system containing about 350 ml whole blood from each of 8 different donors was used in vitro. Each of the eight test-runs also contained 1000 U added heparin. The dialysis procedure was performed using hemophan membranes (GFS + 12, Gambro) with bicarbonate and potassium 3.0 (D210, Gambro) as dialysate. Two electric poles were placed in the blood line, before and after the dialyzer (connected in parallel) and the ground was placed at entry and exit of the dialysate fluid coming from the machine to the dialysis filter. C3d was measured before the start of "dialysis" and at 15, 30, 45 and 60 min, during dialysis. Thereafter the 1.5 mA current was switched on and additional samples were drawn at 75 and 90 min. The mean C3d values were calculated. Paired non-parametric statistical analyses were performed. RESULTS: There was a significant and continuous increase in C3d as compared to the "predialysis" level. The increase during 0 to 30 minutes was greater than that from 30 to 60 minutes (p=0.018); the increase in C3d during 60 to 90 min, was greater than that from 30 to 60 min (p=0.018) and there was no difference between the 0 to 30 and the 60 to 90 min increases. CONCLUSIONS: A current, used in this study, was able to induce a blood membrane interaction during in vitro dialysis. Even a weaker current leakage might have such adverse effects and similar interactions seem possible during regular dialysis depending on the extent of the leakage.

Complement Activation↗
PubMed1988

Structural and functional analysis of CR2/EBV receptor by means of monoclonal antibodies and limited tryptic digestion.

The receptor for the C3d fragment of the third component of complement, CR2, has recently been shown also to act as the receptor for the Epstein-Barr virus (EBV) and to be involved in the control of B-cell proliferation. In order to define functionally important domains on this molecule, we produced monoclonal antibodies to several distinct epitopes. CR2 was purified from a NP-40 lysate of human tonsils by a new method involving sequential chromatography on lentil lectin Sepharose 4B and DEAE-Sephadex and used to immunize mice. After fusion we obtained four stable hybridoma lines producing antibody to CR2. Specificity of these antibodies for CR2 was ascertained by immunofluorescence analysis on a panel of various cells known to possess CR2, by their reactivity in a recently described ELISA for C3 receptors, by Western blotting with purified CR2 and immunoprecipitation from 125I-labelled Raji cells. These four antibodies were found to recognize three distinct epitopes localized on the same fragments of 95,000, 72,000, 50,000, 32,000 and 28,000 MW obtained after mild tryptic digestion of CR2. The 72,000 MW fragment contains the binding site for C3d. Two monoclonal antibodies recognizing the same epitope did not inhibit the binding of C3d-coated sheep erythrocytes to Raji cells, whereas the other two antibodies against distinct epitopes did inhibit in the presence of a second antibody. All four monoclonal antibodies stimulated the proliferation of human peripheral blood B cells.

Antibodies, Monoclonal↗
PubMed1996

Ligation of the functional domain of complement receptor type 2 (CR2, CD21) is relevant for complex formation in T cell lines.

We investigated the potential of CD21, the complement receptor type 2, to form receptor complexes with other membrane molecules on T cell lines. CD21 from T cell lines transformed with human T cell leukemia virus type I (MT2, HUT-102, C5.MJ, Mondi, and C91.PL) and T cell lines that were not virus transformed was analyzed by coprecipitation following cell lysis with digitonin. mAbs binding to functional and nonfunctional epitopes of CD21 and a polyclonal antiserum against its intracellular portion precipitated CD21, which was indistinguishable from CD21 on B cell lines. In contrast to B cells, where CD21 is complexed with CD19 and CD81 (target of anti-proliferative Ab 1) or, alternatively, with CD35 (CR1), no surface molecules could be coprecipitated with three of four mAbs from these T cell lines. Therefore, we assume that CD21 is not part of a preformed complex in T cell lines. OKB7, the only mAb directed against the functional C3d binding site, coprecipitated two proteins of 105 and 55 Mr with CD21 from MT2 and Mondi cells and from the T cell lines Jurkat E6-1 and SupT1. These bands were also recovered with CD21 precipitated from MT2 cells with C3d bound to Sepharose via the internal thioester, but were absent in CD21-expressing B cell lines. As C3d and OKB7 are functional ligands for B cells, we propose that upon ligation on T cells, CD21 associates with molecules of 105/55 Mr in the plasma membrane. Whether this is the first event of a signal delivered to the T cell is under current investigation.

Antibodies, Monoclonal↗
PubMed2006

Expression of complement regulators and receptors on human NT2-N neurons--effect of hypoxia and reoxygenation.

Complement activation can cause tissue damage in cerebral stroke by the release of biologically potent activation products and impaired function of regulatory proteins. We investigated the constitutive and hypoxia-reoxygenation-dependent expression of complement receptor 1 (CD35), membrane cofactor protein (CD46), decay-accelerating factor (CD55), protectin (CD59), and complement C3a and C5a receptors (C3aR and C5aR) on human NT2-N neurons. The effect of hypoxia-reoxygenation on C3d-deposition on neurons and endothelial cells was also investigated. NT2-N neurons were examined by cellular enzyme-linked immunosorbent assay and immunofluorescence microscopy. Endothelial cells were examined by flow cytometry. Three hours 1% or 0.1% hypoxia and 21h reoxygenation with 50% AB-serum were used to investigate the effect of hypoxia-reoxygenation on regulators and C3d-deposition. NT2-N neurons expressed significant amounts of CD59 (Clone H19/Clone BRIC229: p=0.000006/p=0.000003), CD46 (p=0.00006), CD55 (p=0.003) and C3aR (p=0.00003). CD35 and C5aR were not significantly expressed. There were no effects of hypoxia-reoxygenation on any of the regulators or receptors after 1% hypoxia and reoxygenation. However, CD55 (p=0.02) was down-regulated after 0.1% hypoxia and subsequent reoxygenation with AB-serum. There were no difference observed in the C3d-deposition during hypoxia-reoxygenation in either neurons or endothelial cells. In conclusion, human NT2-N neurons constitutively express C3aR, CD46, CD55 and, in particular, CD59. The cells may respond to locally produced C3a and, at the same time, be well protected against complement attack. Although severe hypoxia-reoxygenation may down-regulate CD55 expression, it does not seem to influence C3d-deposition.

Cell Hypoxia↗
PubMed1996

Identification and characterization of complement C3 receptors on human astrocytes.

Astrocytes express C components and have been implicated as a major source of intrathecal C. To ascertain the effects of C activation on these cells, we have evaluated the expression of CR1, CR2, and CR3 (CD35, CD21, and CD11b/CD18) in primary fetal astrocytes and astrocyte cell lines. None of the astrocyte cells tested expressed CR3, whereas primary astrocytes and one of four astrocyte cell lines expressed CR1 (220 kDa), as assessed at the protein and mRNA level. Primary fetal astrocytes and all four astrocyte cell lines expressed CR2 (155 kDa). Expression of CR2 by astrocytes was confirmed at mRNA level by reverse-transcriptase PCR, using different combinations of seven specific CR2 oligonucleotides, and by partial sequencing of the astrocyte CR2 cDNA. Astrocyte CR2 cDNA presented 100% homology with the lymphocyte CR2 cDNA between the position 181 bp to 600 bp and position 1017 bp to 1347 bp. An alternative splicing pattern of exon 11, reported previously in B cells, was observed in astrocyte CR2 cDNA. Astrocyte CR2 was functional, in that it specifically bound C3d and the EBV surface protein gp340, and the binding was blocked specifically with polyclonal anti-CR2. Scatchard analysis of membrane expression of CR2 on astrocytes revealed 2000 functional sites per cell with a Kd (3 x 10(-7) M) identical with that of CR2 on B cell (Raji).

Astrocytes↗
PubMed2000

The role of complement in B cell activation and tolerance.

It is becoming well accepted that innate immunity serves as a natural adjuvant in enhancing and directing the adaptive immune response. In this review, I have discussed how the complement system, a major mediator of innate immunity, links the two systems. The recent availability of knockout mice bearing selective deficiencies in the critical complement proteins and receptors has allowed formal demonstration of the importance of complement in enhancement of humoral immunity. Characterization of the mice has also uncovered mechanisms for maintaining survival of activated B cells within the lymphoid compartment. For example, co-ligation of the CD21/CD19/Tapa-1 receptor with the BCR not only reduces the threshold for B cell follicular survival but provides a unique signal for survival in the germinal centers. In addition complement receptors are critical for localization of antigen and C3d ligand to FDCs for maintenance of long-term B cell memory. A surprise that has come from analysis of the deficient mice is that complement is also important in negative selection of B lymphocytes. This observation provides new insight to a long-standing enigma that the major predisposing factor in lupus is deficiency in complement C1q or C4. The seeming contradiction of dual role for complement in both B cell activation and tolerance is reconciled by the hypothesis that natural IgM provides a mechanism to selectively identify self-antigens that are highly conserved and cross-react with microbial ones such as DNA and nuclear proteins. Thus, the importance of complement in tolerance to self-antigens is restricted to those self-antigens that are evolutionary conserved, and they are identified by natural antibody. The future should hold further surprises as to the intricate interactions between the complement system and acquired immunity.

Adjuvants, Immunologic↗
PubMedDate not supplied

Prevalence of circulating immunecomplexes and variations of complement fractions in HBV, HDV and HCV infections: statistical analysis and clinical correlations.

Increased levels of circulating immunecomplexes (CIC) have been demonstrated in the serum of patients with HBV infection and HDV superinfection. This finding appears to be correlated to the disease's activity. In this report serum levels of two fractions of CIC (CIC-Clq and CIC-C3d) were evaluated by ELISA method in a sample of 110 subjects with hepatitis infection (HBV, HCV, HDV). Reference values were obtained in a group of 45 healthy subjects (blood donors). Both the CIC fractions were increased in the patients with HCV infection. The most significant increase for both CIC-C1q and CIC-C3d was found in the cirrhotic patients. The complement fractions C3c and C4 were determined in the serum of these patients to investigate a potential pathogenic role of such immunecomplexes. C3c and C4 fractions showed a significant decrease only in the cirrhotic patients, without correlation with the viral agent. Serum levels of C1q complement fraction were not significantly decreased, thus excluding an impaired synthesis of complement fractions. No significant correlation was found between CIC and C3c and C4 fractions in patients with increased levels of CIC, except a slightly significant correlation between reduction of C3c and increase of CIC-C1q. These data suggest a pathogenic action of immunecomplexes in the course of HCV, particularly in the cirrhotic stage.

Adult↗
PubMed1993

The serum complement system in children on continuous ambulatory peritoneal dialysis.

OBJECTIVE: During continuous ambulatory peritoneal dialysis (CAPD), the loss of complement factors via the dialysate may cause complement deficiencies. This hypothesis was tested in a group of children treated with CAPD. DESIGN: Classical (CH50) and alternative (AP50) complement activity and serum levels of factors C1q, C3, C4, C3d, B, D, and P in CAPD patients were compared to normal controls and to children with preterminal renal failure. SETTING: Patients were seen in a university hospital; normal controls were seen in an outpatient clinic of a general hospital. PATIENTS: A group of 22 children on CAPD was compared to a normal control group of 44 children and to a group of 12 children with preterminal renal failure with a creatinine clearance below 25 mL/min/1.73 m2. RESULTS: CH50, AP50, C3, and B were not significantly different from the control group in both the CAPD and preterminal groups. Factors C1q (p = 0.01) and C4, C3d, D, and P (p < 0.001) were higher in the CAPD group in comparison to the normal control group. The factors D (p < 0.001) and P (p = 0.02) were also elevated in the preterminal group. For the measured factors there was no significant difference between the CAPD group and the preterminal group. CONCLUSIONS: There is no deficiency of complement in children treated with CAPD. High levels of C3d and D can be explained by the reduction of their elimination by the kidney. The increased levels of the other factors are presumably due to increased synthesis in renal failure. This does not seem to be caused by CAPD.

Adolescent↗
PubMed1981

[Immune complexes and complement in leprosy (author's transl)].

The sera of 87 Senegalese patients with various forms of leprosy were investigated. Two of the most reliable methods were used to detect circulating immune complexes : the radiolabelled C1q binding test and the Raji cell binding technique. Several fractions of complement, including C3, C4, factor B and the C3d product of C3 were also assayed. A material having the properties of immune complexes was detected in lepromatous and reactional leprosy. In tuberculous leprosy, only the Raji cell binding technique gave positive results. C3 and C4 were normal or slightly raised, but C3d was increased in all forms of the disease. There was no significant correlation between C3d values and the results of immune complexes detection tests.

Antigen-Antibody Complex↗
PubMed1984

Measurement of fragments of the third component of human complement on erythrocytes by a new immunochemical method.

This paper describes a new antiglobulin consumption method to quantitate the fragments of the third component of human complement (C3) on red blood cell (RBC) membranes. Zymosan-bound C3, which can be stored frozen at -80 degrees C for years, was used as a standard in these tests. Using anti-C3c antibody, zymosan-bound C3 could be calibrated against soluble converted C3 (beta 1A), but not against soluble, native C3 (beta 1C). Calibration with several commercial serum standards yielded virtually identical values. Approximately 79.8 +/- 28.2 C3d molecules (mean +/- 1 SD, n = 50) were detected on normal, freshly collected RBC by this method, whereas no C3c fragments were noted. EC43, prepared by dilution of blood samples with low ionic strength solution, had between 650 and 3,100 C3 molecules/RBC when measured with anti-C3c and between 1,140 and 6,500 C3 molecules when measured with anti-C3d. These data indicated that part of the C3b molecules on EC43 had cleaved to C3d. EC43 are reported to have up to 200,000 C3 molecules when measured by other techniques. To resolve this discrepancy, EC43 were prepared by dialysis of blood samples against low ionic strength solution. About 97.5% of C3 remained in plasma after dialysis supporting the results of our tests. The new assay is an accurate and sensitive method of quantitating C3 fragments bound to RBC in vivo and in vitro.

Binding Sites, Antibody↗
PubMed1980

Release of endogenous C3b inactivator from lymphocytes in response to triggering membrane receptors for beta 1H globulin.

Human bone marrow-derived lymphocytes and cells from B lymphoblastoid lines were shown to have specific membrane receptors for beta 1H globin. Lymphocytes responded to the presence of beta 1H by releasing endogenously-synthesized C3b-inactivator. Very little spontaneous release of C3b-inactivator occurred in the absence of beta 1H. beta 1H-treated lymphocytes that either lacked complement receptor type one (CR1, the C4b-C3b receptor) or had their CR1 blocked with Fab'-anti-CR1 formed rosettes with C3b-coated sheep erythrocytes (EC3b) by adherence to complement receptor type two (CR2, the C3d-C3bi receptor). The mechanism of the beta 1H-induced EC3b rosette formation was shown to involve the release of lymphocyte C3b-inactivator that cleaved bound C3b into C3bi forming EC3bi. This lymphocytes-generated EC3bi then bound to CR2, forming rosettes. beta 1H-induced EC3b rosettes were completely inhibited by the presence of either anti-C3b-inactivator, F(ab')2-anti-CR2, Fab-anti-C3c, or Fab-anti-C3d, but were unaffected by the presence of fluid-phase concentrations of beta 1H up to 5.5 mg/ml or Fab'-anti-CR1. Analysis by sodium dodecyl sulfate polyacrylamide gel electrophoresis and fluorography demonstrated that cell-free supernates of beta 1H-treated lymphocytes cleaved 3H-labeled C3b on EC3b into C3bi. Inhibition studies with chelating agents and sodium azide suggested that the release of C3b inactivator might involve a calcium and energy-dependent transport of this enzyme across the membranes of beta 1H-triggered cells. Because plasma beta 1H and C3b-inactivator are known to have important functions in the distinction of alternative pathway-activating substances from normal tissue, it is possible that this beta 1H receptor-C3b-inactivatory releasing system in lymphocytes may have an analogous function.

B-Lymphocytes↗
PubMed1983

Immunopathological studies of polyarteritis nodosa and Wegener's granulomatosis: a report of 43 patients with 51 renal biopsies.

Although it is generally considered that vasculitis of the polyarteritis nodosa (PAN) group and Wegener's granulomatosis (WG) is immune complex (IC) mediated, there are no simultaneous data on circulating IC, complement levels and deposits of Ig and complement in the kidney. Therefore we have performed a retrospective study of 43 patients suffering from PAN and WG. Ig glomerular deposits were uncommon and scanty, except in two patients with WG; C3 deposits were detected in 12 patients, whereas fibrinogen was constantly found when lesions were recent and active. Similar data were obtained for the renal vessel walls. Contrasting with these results, rheumatoid factors and cryoglobulins, suggestive of the presence of circulating IC, were detected respectively in nine of 39 and seven of 37 patients, and IC 'activity' assessed by the Raji cell assay and the Clq binding assay was found respectively in six of 17 and nine of 10 patients before treatment, and in none of 10 and five of seven patients in remission. Haemolytic complement activity and complement components were never decreased, but the C3d breakdown product of C3 was elevated in all the eight patients studied before treatment. Signs of persistent hepatitis B virus (HBV) infection were detected in five of 25 patients of the PAN group, whereas three of eight patients with WG had only anti-HBV antibodies. Furthermore, cytomegalovirus (CMV) could be isolated from the blood in a case of WG before the treatment was started. Persistent interferonaemia was detected in one of five patients. These results suggest either that renal deposition of CIC is transient, the paucity of Ig deposits being due to rapid clearance of IC by phagocytic cells; or alternatively that vascular and glomerular lesions are not caused by CIC, as in some cases of experimental vasculitis induced by infectious agents.

Adolescent↗