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Complement receptors in human renal glomeruli.
Glomeruli in Cryostat sections of foetal and adult renal tissues adsorbed sheep erythrocytes sensitized with IgM antibody and human or mouse complement (EAC). Activated complement was essential for the reaction to occur. The receptor had specificity for the C3b fragment of C3 and is probably of protein or glycoprotein nature. Complement receptors in glomeruli may explain the deposition of complement components or complement-containing complexes in immune-complex glomerulonephritis.
Activation of complement by DMSO and ethanol and its inhibition by soluble complement receptor type 1.
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Complement receptor enhancement by chemotactic factors.
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Use of fluoresceinated complement-coated bacteria and sheep erythrocyte-antibody-complement complexes for identification of complement receptors on lymphoid cell lines: differences in binding characteristics between cell lines of normal and malignant origin.
Twenty-four lymphoma-derived cell lines, 11 cord blood lymphocyte lines, and 3 lymphoblastoid cell lines derived from normal adults were examined for complement (C) receptors utilizing fluoresceinated C-coated bacteria (FBC) to determine the optimal conditions for each type of cell line. Incubation of FBC with lymphoma-derived cell lines at 37 and 0.5 degrees C showed that maximal FBC binding at both temperatures was after 120 minutes, and peak reactivity was invariably higher at 37 degrees C. These temperature-dependent differences were similar, both in Epstein-Barr virus nuclear antigen (EBNA)-positive and EBNA-negative lines. EBNA-positive lines, however, expressed higher levels of FBC rosettes than EBNA-negative lines at both temperatures. In contrast, FBC binding to cord blood cell lines after 120-minute incubation was maximal at 0.5 degrees C. Although similar numbers of FBC rosettes were formed after 30 minutes at both 37 and 0.5 degrees C in cord blood cell lines, rosette formation deteriorated after longer periods of incubation at 37 degrees C. The optimal temperature for FBC binding to lymphoblastoid cell lines could not be determined, since bacteria bound spontaneously to these lines at 37 degrees C. Cell lines were also tested simultaneously for sheep erythrocyte-antibody-complement complex (EAC)M and FBC binding at 37 and 0.5 degrees C. FBC reactivity under optimal conditions for each type of cell line correlated well with EACM reactivity at 37 degrees C. The significance of these results is discussed.
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.
Critical role for complement receptor 3 (CD11b/CD18), but not for Fc receptors, in killing of Streptococcus pyogenes by neutrophils in human immune serum.
During phagocytosis, surface receptors on neutrophils interact with pathogens opsonized with complement factor C3b/iC3b and in some cases with antibodies. In human immune sera antibodies directed against surface-bound M proteins mediated killing of Streptococcus pyogenes by neutrophils. Surprisingly, blocking of the Fc receptors had little effect on the killing. In contrast, inhibition of C3b/iC3b generation, or blocking of the major neutrophil iC3b receptor CD11b/CD18, enabled S. pyogenes to grow efficiently in immune sera. Inhibition of CD11b/CD18, but not of CD32, the major neutrophil signaling Fc receptor, prevented Streptococcus-induced NADPH oxidase-dependent respiratory burst, and blocking of C3b/iC3b formation inhibited Streptococcus-induced activation of Cdc42, a small GTPase critically involved in transmitting pro-inflammatory signals to the cytoskeleton. Consequently, ligation of CD11b/CD18 by bacteria-bound iC3b is necessary for inducing a neutrophil response leading to elimination of S. pyogenes in immune human serum.
Complement receptors and histamine degradation.
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Complement activation and complement receptors in systemic lupus erythematosus.
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Surface expression of complement receptor gC1q-R/p33 is increased on the plasma membrane of human spermatozoa after capacitation.
Evidence is increasing that complement components might play a role in fertilization. C1q, the first component of the classical complement cascade, has the ability to promote sperm agglutination in a capacitation-dependent manner as well as an effect on sperm-oolemma binding and fusion. We have previously detected gC1qR, the receptor for the globular head portion of C1q, on the surface of capacitated sperm. In this study, we examined the expression of gC1qR in both fresh and capacitated human spermatozoa. We performed immunoprecipitation for gC1qR and analyzed biotinylated sperm membrane by Western blot to illustrate an increase in receptor density after overnight capacitation. These results were confirmed by flow cytometric analysis of spermatozoa using fluorescein isothiocyanate-labeled monoclonal anti-gC1qR antibody. Confocal, indirect immunofluorescence microscopy revealed an increase in receptor expression over the rostral portion of the sperm head after capacitation. In addition, the ability of live spermatozoa to bind to monoclonal anti-gC1qR antibody-coated microtiter wells was also increased after capacitation. These results suggest that gC1qR may play a role in human fertilization.
Impairments in complement receptor- and Fc receptor-mediated functions in vivo in patients with psoriasis.
The function of the fixed macrophage system in 18 psoriasis patients was evaluated by measuring the elimination rate of injected autologous erythrocytes coated with iC3b or IgG. The mean half-life of iC3b-coated erythrocytes was significantly prolonged in patients with psoriasis compared with healthy controls (4.7 +/- 0.8 vs 2.7 +/- 0.2 min, P = 0.01). There was also a decrease in the total number of cells eliminated from the circulation (2.5 +/- 0.2 x 10(8) vs 3.3 +/- 0.2 x 10(8), P = 0.01). There was an even more pronounced increase in the half-life of IgG-coated erythrocytes (85 +/- 18 vs 20 +/- 5 min, P < 0.001), with normal values in only 5 of 15 patients, and 4 of these 5 patients were receiving systemic treatment. The slow elimination was interpreted as being caused by primary or secondary defects in receptor function rather than by blocking of the receptors by immune complexes, since patients with psoriasis show normal levels of circulating immune complexes. Further studies are needed to elucidate the nature of these defects.
Complement receptors CR1 on human peripheral nerve fibres.
Receptors for C3 and C4 in human peripheral nerve tissue were studied by examining the adherence of complement (C) coated erythrocytes (E) and by using monoclonal antibodies against epitopes on the receptors for C3b (CR1), C3d (CR2) and C3bi (CR3). E (erythrocyte)-bearing C3b or C4b adhered to sections of myelinated peripheral nerves and the binding was inhibited only by anti-CR1 antibodies. By immunofluorescence, anti-CR1 antibodies stained the nerve fibres, whereas anti-CR2 and anti-CR3 antibodies did not. The staining was apparently localized to the Schwann cell membrane. E-bearing C3bi or C3d did not adhere to myelinated or unmyelinated nerves. CR1 are therefore the only C3 receptors expressed in human peripheral nerves. E-bearing C3b or C4b did not adhere to unmyelinated nerves from adults or to nerves from fetuses at a gestational age of approximately 21 weeks, whereas monoclonal anti-CR1 antibodies stained myelinated, unmyelinated and fetal nerves equally well. The results indicate that CR1 in unmyelinated and fetal nerves are either functionally inactive or express a lower affinity for C3b/C4b than CR1 in myelinated nerves. There were no significant differences in the binding of E-bearing C3b or C4b to myelinated peripheral nerves from 50 individuals, indicating that CR1 activity is not distributed phenotypically.
Complement receptor type 2 mediates infection of the human CD4-negative Raji B-cell line with opsonized HIV.
Opsonization of the HTLV-RF and HTLV-IIIB strains of HIV-1 with normal human HIV seronegative serum under conditions that allow complement activation resulted in the productive infection of cells of the Raji B lymphoblastoid cell line. Under the same experimental conditions, no infection of Raji cells was observed with unopsonized virus. Infection of Raji cells with complement-opsonized HIV-1 was totally suppressed by preblocking the function of CR2 (the C3dg receptor, CD21) on the cells with a monoclonal anti-CR2 antibody cross-linked with rabbit F(ab')2 anti-mouse immunoglobulin antibodies. Infection of Raji cells occurred independently of CD4 since the cells lacked the expression of CD4 antigen and of CD4 transcripts. Thus, Raji cells may be infected with complement-opsonized HIV independently of CD4 and in the absence of antibodies. By mediating and/or enhancing HIV infection, complement and complement receptors contribute to extend the range of target cells to the virus and may increase infection in patients with a low viral load.
Fc- and complement-receptor activation stimulates cell cycle progression of macrophage cells from G1 to S.
Phagocytosis of microorganisms by macrophages is an important host defense mechanism. While studying the phagocytosis of the human pathogenic fungus Cryptococcus neoformans, we noted that macrophage-like J774 cells with ingested fungal cells had frequent mitotic figures. By analyzing the relative proportion of phagocytic cells as a function of cell cycle phase, we observed an increase in S phase cells after Fc-mediated phagocytosis of polystyrene beads, live or heat-killed C. neoformans. This result was confirmed by increased nuclear BrdU incorporation after Fc-mediated phagocytosis. The induced progression to S phase was observed after both Fc- and complement-mediated phagocytosis of live yeasts. Fc-mediated stimulation of cell division did not require ingestion, because it could be triggered by incubating cells in IgG1-coated plates. Phagocytosis-mediated stimulation of replication was confirmed in vitro using primary bone marrow macrophages and in vivo for peritoneal macrophages. We conclude that phagocytosis of microbes or inert particles can stimulate macrophages to enter S phase and commence cell division. This observation suggests a potential mechanism for increasing the number of effector cells after microbial ingestion, but can also promote the spread of infection.
Trypan blue inhibition of complement receptor function on various cells.
Trypan blue has previously been shown to inhibit complement-mediated phagocytosis by interaction with the C3 receptor but not with the Fc receptor. In studies reported here, trypan blue inhibited EAC3 rosette formation with human polymorphonuclear leucocytes (PMN) and mononuclear cells, rabbit alveolar macrophages (AM) and peritoneal PMN, and guinea-pig spleen cells. Trypan blue also inhibited C3-mediated bacterial adherence to the same receptor-bearing cells and to human glomerular cells. EAC3bi rosette formation was also inhibited, but EAC3d rosettes were not detected in our assay system. Although the precise molecular nature of C3b fragments deposited on antibody-sensitized erythrocytes has not been fully determined, trypan blue probably inhibits all C3 receptors from different species and may prove useful in vivo and in vitro for the definition of C3-receptor function in various aspects of the immune response.
Characterization of Ia8 antigen, thy-1.2 antigen, complement receptors, and virus production in a group of murine virus-induced leukemia cell lines.
Ia8, a cell membrane antigen controlled by gene(s) located in the I region of the H-2 complex, was found on 9 of 26 murine leukemia cell lines. Iaddition, 3 of the 9 Ia8-bearing lines had a membrane receptor for antigen-antibody-complement complexes. Six of 26 lines bore the Thy-1.2 antigen. Ia8 and Thy-1.2 antigens were mutually exclusive on the cell lines studied. The strain of virus used to induce the leukemia, the H-2 type of the cells, and the techniques of leukemia cell propagation all appeared to influence the antigenic characteristics of the cell lines obtained. Production of infectious murine leukemia virus in vitro and expression of leukemia virus-induced membrane antigens did not appear to correlate with the presence of I8 or Thy-1.2 antigens or with the H-2 type of the cells.
Soluble complement receptor one (sCR1) inhibits the development and progression of rat collagen-induced arthritis.
We set out to determine whether inhibition of complement using sCR1 could influence the development and progression of collagen arthritis in the Lewis rat. Collagen arthritis was successfully established in the Lewis rat, using a novel immunization schedule. In separate experiments, cobra venom factor (CVF) and sCR1 were used to achieve systemic complement inhibition. Their respective effects on disease onset and on the progression of established disease compared with saline-treated control animals was explored. Arthritis was assessed by measurement of clinical score, paw diameter and paw volume. Complement inhibition using either CVF or sCR1, prior to the onset of clinical signs of inflammation, delayed the development of disease. CVF was ineffective in the treatment of established disease, whereas sCR1 delayed the progression of disease in affected joints and prevented the recruitment of further joints while the animals were complement-depleted. In the control saline-treated groups the disease continued to progress relentlessly. We conclude that complement activation is important in the initiation and maintenance of inflammation in collagen arthritis. The potent disease-modulating effect of sCR1 provides persuasive evidence that specific complement inhibiting agents may be an effective approach to the treatment of inflammatory joint diseases
Macrophage heterogeneity in the rat as delineated by two monoclonal antibodies MRC OX-41 and MRC OX-42, the latter recognizing complement receptor type 3.
Two monoclonal antibodies, designated MRC OX-41 and MRC OX-42, have been shown to label subsets of macrophages. Using immunoperoxidase and immunofluorescence analysis, tissue macrophages were shown to be heterogeneous with respect to binding of MRC OX-41 and MRC OX-42 antibodies. Although both antibodies labelled subsets of macrophages, the antibodies also reacted with granulocytes and dendritic cells. The antigens recognized by these antibodies were identified by metabolic and cell surface labelling followed by immunoprecipitation and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). MRC OX-41 recognized a surface protein of 110,000-120,000 MW, while MRC OX-42 immunoprecipitated three polypeptides with molecular weights of 160,000, 103,000 and 95,000. The Fab fragment of MRC OX-42 antibody inhibited complement-mediated rosette formation between sensitized erythrocytes and rat macrophages and granulocytes. Membrane molecules with similar biochemical and functional properties to MRC OX-42 antigen have been identified in mouse and man as the receptors for iC3b, and it is probable that MRC OX-42 antibody recognizes the rat homologue of the receptors in these other species.