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PubMed1991

Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin.

Human keratinocytes are able to synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system (CD16, CD36, HLA-DR, intercellular adhesion molecule-1). In the present study, skin biopsies from healthy volunteers, from patients with psoriasis vulgaris (PV), mycosis fungoides (MF), purpura pigmentosa chronica (PPC), acute urticaria (AU) and from positive tuberculin skin tests were investigated with regard to the reactivity with the monoclonal antibodies to complement receptors CR1 CR2 and CR3 by means of a multistep immunoperoxidase method. In the clinically involved skin of all patients with PV, MF or PPC, and in biopsies obtained from positive tuberculin tests, specific epidermal intercellular staining with OKB7 and Leu anti-CR2 was seen on subcorneal keratinocytes. This finding suggests a differentiation-linked expression of CR2 on human keratinocytes in cytokine-mediated skin diseases whereas CR1 and CR3 are apparently not expressed.

Antigens, CD↗
PubMed1981

Quantitation of red blood cell-bound C3d in normal subjects and random hospitalized patients.

A sensitive radiolabelled anti-antiglobulin method was devised and applied to quantitating red blood cell-bound C3d (RBC-C3d) in samples from 174 normal blood donors. C3d was demonstrable on all RBC examined; 98% of values fell over a broad range, with the highest values being approximately 3.5 X the lowest values (equivalent to 50-160 molecules of C3d per cell). RBC-C3d did not correlate with sex or age (over 18-65 years); indirect evidence suggests that values for the paediatric age group will fall in the same normal range. Studies on samples obtained weekly for 10-12 weeks from six adult males and six adult females indicated stable levels of RBC-C3 for individual subjects; i.e. high normals, mid normals and low normals remained in their characteristic range levels over the period of observation. For comparison, RBC-C3d was measured in samples from 313 randomly selected hospitalized adult patients. 33% of the values were above the normal range; 8% were elevated to a level likely to have been detectable by a direct anti-C3d antiglobulin test. The great majority of elevated values occurred in patients not ordinarily considered to have autoimmune conditions. The results provide background for studies of the aetiology and significance of RBC-C3d in health and disease.

Adult↗
PubMed1986

Changes of serum complement concentrations in tumour patients prior and after radiotherapy.

Peripheral blood concentrations of leucocytes, platelets and complement factors Clq, C3c, C3d, C4 and C5 were examined in 30 patients suffering from malignant tumours prior and after radiotherapy. In general, a decrease of blood cell concentrations as well as serum complement levels was noted using regression analysis. Two groups were formed: patients with (group I) and without (group II) foregoing tumour surgery. A positive correlation was found for all complement factors prior therapy in group I, whereas only some complement components did correlate in group II. The results in group I are in agreement with complements classical pathway activation. We conclude that the alternative pathways influence is responsible for the different results in group II.

Combined Modality Therapy↗
PubMedDate not supplied

Early steps in fusion between Epstein-Barr virus and a human hepatoma cell line (Li7A).

Epstein-Barr virus, the causative agent of mononucleosis and several human cancers, infects cells via complement receptor type 2 (CR2). Expression of this receptor is restricted to B lymphocytes, some epithelial cells and immature thymocytes; expression of CR2-like proteins has been also found on T cells. In the present report, we identified the presence, on the membrane of Li7A cells, of a novel EBV receptor distinct from CR2 capable of triggering fusion with EBV virions with more rapid kinetics than that found with lymphoblastoid cells (Raji).

Carcinoma, Hepatocellular↗
PubMed1988

Immunohistochemical study of Warthin's tumour with special regard to the germinal centre.

In order to analyze the role of the lymphoid stroma of Warthin's tumour, the author made an immunohistochemical study especially focussing on the germinal centre (GC). In the GCs, IgM and IgE were much more clearly observed in a lace-like network than other heavy chains, and also could be detected electron microscopically on the surface of GC cells and follicular dendritic cells (FDCs). Plasma cells scattered beneath the epithelial component were mainly positive for IgG and IgA. IgG-positive plasma cells were more predominant than IgA plasma cells. Among the cases examined, there was a significant difference in the number of IgE-positive GC and plasma cells. In the GCs five complement components (C1g, C4, C3c, C3d, C5) and complement receptors (C3bR and C3dR) were positive, displaying a lace-like pattern, which were proved, electron microscopically, to coincide with the surface of FDCs and GC cells. IgE-positive GCs showed the same result. DRC1, which specifically reacts to FDC-membrane, was located only in GCs, and electron microscope also revealed positive findings on the surface of FDCs. The above mentioned findings in the GC of Warthin's tumour were similar to those of lymph nodes except for the frequent distribution of IgE. Salivary amylase was seen in the GC on rare occasions, but was not positive on the surface of GC cells and FDCs. It is suggested that FDCs play an important role in immunological behaviour with complement and complement receptors in the GC of Warthin's tumour.

Adenolymphoma↗
PubMed1987

Activation of human platelets through gp140, the C3d/EBV receptor (CR2).

gp140, the C3d/EBV receptor (CR2), previously isolated and characterized from human B lymphocytes, was identified on human platelets: by measuring the specific binding of either polyclonal anti-gp140 IgG and monoclonal anti-C3d/EBVR antibodies, as OKB-7 and HB-5, or human C3d; by isolating gp140 from solubilized platelet components with polyclonal anti-gp140 IgG or monoclonal OKB-7, using immunoprecipitation and electro-immunoblotting assays; by inducing specific activation of human platelets. Cross-linking of this receptor by polyclonal anti-gp140 IgG induced aggregation of human platelets and stimulated ATP release. Absence of lactate dehydrogenase release and inhibition by EDTA and prostacyclin of anti-gp140-induced aggregation, support strongly active aggregation and absence of lysis. Platelet aggregation by anti-gp140 required metabolic activities and was modulated by fibrinogen, paf-acether or thrombin. OKB-7 triggered human platelet aggregation when cross-linked by anti-mouse second-step antibodies. In the same way, platelet activation by C3d fragment was detected, in presence of fibrinogen, only when C3d was cross-linked on the cell surface by anti-C3d F(ab')2 fragments.

Adenosine Triphosphate↗
PubMed1982

C3c and C3d fragments of human C3 bind myeloma IgG1 and IgG3 proteins.

Eight human myeloma proteins, two of each IgG subclass, were studied for binding to solid-phase C3c and C3d by the ELISA technique. Myeloma IgG1 kappa, IgG1 lambda, IgG3 kappa and IgG3 lambda proteins bound to C3c and C3d, while two IgG2 kappa, and two IgG4 kappa proteins failed to show significant binding affinity. The results suggest that like C1q, the stable binding sites of C3, located on the C3c and C3d parts of the molecule, have affinity for IgG subclasses 1 and 3.

Animals↗
PubMed1989

The influence of C3-coated homologous erythrocytes on pokeweed-mitogen-induced polyclonal differentiation of human B cells.

The present study was undertaken in order to test the hypothesis that homologous erythrocytes (E) coated in vivo with C3d could modulate the immunoglobulin (Ig) synthesis of human peripheral blood mononuclear cells (PBMC), stimulated with pokeweed mitogen (PWM) in vitro. E from healthy individuals were found to enhance markedly the Ig synthesis of PMBC cultures stimulated with suboptimal doses (0.01 microgram/ml) of PWM. E coated in vivo with increasing amounts of C3d (1.4-6.3 times the amounts on normal E), obtained from patients with systemic lupus erythematosus, failed to induce any significant increase in Ig synthesis of PBMC cultures stimulated with suboptimal PWM doses, compared with cultures co-stimulated in parallel with normal E. In contrast, an increase in IgM and IgG synthesis was observed in about 50% of PBMC cultures from different donors when stimulated with PWM in the presence of E coated with C3b in vivo (from a patient with congenital factor I deficiency), compared with the Ig synthesis in cultures co-stimulated in parallel with normal E. In contrast to the inability of C3d-coated E to modulate B-cell proliferation, the monoclonal anti-CR2 antibody OKB7 was found to be mitogenic for unstimulated peripheral B cells.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1983

Clinical application of a new nephelometric technique to measure complement activation.

A new nephelometric technique to measure C3d as an indicator of complement activation, is described. C3d is isolated at high concentration of polyethyleneglycol (PEG), incubated with commercially available anti-C3d antiserum at a final concentration of 2.5% PEG and then measured in a Behring Laser Nephelometer. In contrast to previously available techniques our assay detects the low concentrations of C3d present in all normal subjects, which result from the continuous C3 catabolism occurring in vivo. We have also measured C3d blood concentrations in a large number of patients with diseases associated with complement activation. Raised C3d concentrations were found in 68% of rheumatoid arthritis, 57% of primary biliary cirrhosis, 38% of chronic active hepatitis, 100% of Gram-negative bacteraemia and 100% of malaria. The nephelometric technique has proved to be sensitive, economical and fast, and could be adapted for routine determination of C3d blood concentrations to monitor disease activity and response to treatment.

Arthritis, Rheumatoid↗
PubMed1998

The role of complement and complement receptors in induction and regulation of immunity.

Covalent attachment of activated complement C3 (C3d) to antigen links innate and adaptive immunity by targeting antigen to follicular dendritic cells (FDC) and B cells via specific receptors CD21 and CD35. Recent characterization of knockout mice deficient in complement components C3, C4, or the receptors CD21 and CD35 as well as biochemical studies of the CD21/CD19/Tapa-1 coreceptor on B cells have helped to elucidate the mechanism of complement regulation of both B-1 and B-2 lymphocytes. Interestingly, natural antibody of the adaptive immune system provides a major recognition role in activation of the complement system, which in turn enhances activation of antigen-specific B cells. Enhancement of the primary and secondary immune response to T-dependent antigens is mediated by coligation of the coreceptor and the B cell antigen receptor, which dramatically increases follicular retention and B cell survival within the germinal center. Most recent evidence suggests that complement also regulates elimination of self-reactive B cells, as breeding of mice that are deficient in C4 or CD21/CD35 with the lupus-prone strain of lpr mice demonstrates an exacerbation of disease due to an increase in autoantibodies.

Animals↗
PubMed1998

Enhanced molecular mimicry of CEA using photoaffinity crosslinked C3d peptide.

Antigen mimicry of using anti-idiotypic antibodies for use as cancer vaccines has been disappointing due to the weak immunogenicity of immunoglobulin variable domains. To enhance the immunogenicity of an anti-idiotype vaccine we incorporated a molecular adjuvant peptide into the antibody. The peptide is derived from the C3d region known to bind CR2 receptors on B-cells. A photoreactive peptide is synthesized that affinity-labels a single site in the antibody variable domain. The molecular adjuvant peptide is crosslinked to the anti-idiotype mimetic by chemical means without modifying other sites on the antibody. The C3d-conjugated anti-idiotype antibody induces a strong idiotype and antigen-specific response in mice.

Adenosine↗
PubMed1990

Expression of the C3d/EBV receptor and of other cell membrane surface markers is altered upon HIV-1 infection of myeloid, T, and B cells.

Human cell lines (the T-cell lines H9, Jurkat, and HUT102, the myeloid lines U937 and HL60, and the Raji B cell line) were infected with HIV-1. HIV-1 antigen could be detected by immunofluorescence analysis in more than 50% of T cells and myeloid cells 15 days after infection. Infection of Raji cells took more than 2-3 months. Studies of cell surface marker expression revealed remarkable changes after HIV-1 infection of Raji cells: expression of CR2 (C3d/EBV receptor, CD19, CD20, CD22, CD23, CD10, and surface IgM) were highly reduced, in the case of CR2 and membrane-IgM from 100 to 0%, whereas levels of CD37 and CD38 remained unaltered by HIV-1 infection. U937 cells showed a reduction of CD4 expression from 14 to 5% after HIV-1 infection; the CR3 expression slightly increased from 25 to 30%. In contrast, HLA-DR was only expressed (21%) after HIV-1 infection but not in uninfected U937 cells. Expression of HLA-DR could be detected also in HL60 cells (33%) after HIV-1 infection. In H9 cells, CD4 was reduced from 60 to 30% after HIV-1 infection, whereas HLA-DR and CD25/IL-2 receptor expression increased from 16 to 90% and from 0 to 50%, respectively. CD4 was reduced from 70 to 0% from Jurkat cells after HIV-1 infection, whereas expression of CR2 was only slightly diminished from 8 to 4%. Expression of CR1 and HLA-DR was slightly increased in these cells (1 to 3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Differentiation, B-Lymphocyte↗
PubMed1984

C3d-K, a kallikrein cleavage fragment of iC3b is a potent inhibitor of cellular proliferation.

The C3d-K fragment generated from human iC3b by plasma kallikrein is a potent suppressant of cellular proliferation. Originally characterized as inhibiting human and murine T lymphocyte function, C3d-K is shown in these studies to suppress mitogen-induced B cell growth, the spontaneous proliferation of several tumor cell lines, as well as all forms of T cell proliferation, including that induced by interleukin 2 (IL 2). In addition, synthesis of IL 2 in mixed lymphocyte cultures is blocked by C3d-K, but not IL 2 synthesis induced by Con A. The C3d-K fragment has no effect on resting cells; however, sensitivity to the inhibitory effect of C3d-K is acquired during the activation process. Because the proliferation of mitogen-activated spleen cells is not inhibited by exposure to C3d-K for the initial 24 hr of culture, only late steps in the cell activation process are C3d-K sensitive. When C3d-K is present throughout the course of the 72-hr culture, suppression was observed. Data obtained with the tumor cell lines suggest that once suppression is achieved, it is long-lasting even in the absence of C3d-K.

Animals↗
PubMed1984

Immunopathological correlation between mesangial C3d-deposition and C3d-fixing circulating immune complexes in lupus nephritis.

By a direct immunofluorescent technique, glomerular C3d deposition was examined in a total of 50 renal biopsy specimens from patients with lupus nephritis. C3d deposition was then compared with disease activity, glomerular IgG and C3c deposition, and the levels of circulating immune complexes (CIC) measured by a solid-phase anti-C3d assay. There was a good correlation between disease activity and the positivity of glomerular C3d deposits (P less than 0.001), as well as C3c deposits (P less than 0.001). Even in clinically inactive patients, a relatively high percentage (59%) of C3d deposits were positive compared with C3c deposits (17%). Mesangial C3d deposition correlated with clinical disease activity more significantly (P less than 0.005) than capillary wall C3d deposition (P less than 0.025). C3d deposits were detected in all of the 30 cases with positive C3c deposits, and moreover, in 15 of the 20 (75%) cases with negative C3c deposits. Glomerular IgG deposits were almost always associated with C3d deposits, both in mesangial areas and along capillary walls, with statistical significance (P less than 0.005, P less than 0.001, respectively). The serum levels of C3d-fixing immune complexes (IC) were significantly correlated with the positivity and intensity of mesangial C3d deposits. This study demonstrates glomerular deposition of C3d in patients with lupus nephritis and reveals a significant correlation between mesangial C3d deposition and disease activity.

Antigen-Antibody Complex↗
PubMed1990

C3d-mediated negative and positive signals on the proliferation of human B cells separated from blood.

Soluble C3d applied to human blood-derived B lymphocytes inhibited anti-mu, T cell-produced growth factor, and EBV-induced DNA synthesis in serum-free culture. C3d added to the B cell cultures 1 and 2 days after the stimulus, still exerted inhibition, though with gradually diminishing efficiency. C3d, fixed on zymosan or attached to the culture wells, induced [3H]thymidine incorporation of the B cells in serum-free medium. The concentration of C3d used to coat the wells was critical, with optimal stimulatory effect of 8.3 micrograms/ml. These C3d molecules were shown to be denatured. Our results are in line with earlier data on B cells derived from mouse spleen and human tonsils showing that depending on the way of presentation and its amounts, the natural ligand of CR2 can exert negative or positive signals. Moreover, we demonstrate that C3d can inhibit even the proliferative stimulus of EBV.

B-Lymphocytes↗