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PubMed1989

Localization of Fc gamma receptors and complement receptors CR1 on human peripheral nerve fibres by immunoelectron microscopy.

The localization of receptors for the Fc part of IgG (Fc gamma R) and for the complement C3b/C4b components (CR1) on human peripheral nerve fibres was investigated by indirect immunoperoxidase staining of frozen nerve sections with monoclonal antibodies. Transmission electron microscopy revealed that Fc gamma R and CR1 are localized to the entire surface membrane and inner membrane (axolemma) of the Schwann cell. Myelin and axons were not stained. The presence of Fc gamma R and CR1 in human Schwann cells adds further evidence for the immunocompetence of these cells.

Animals↗
PubMed1990

The ontogenesis of Fc gamma receptors and complement receptors CR1 in human peripheral nerve.

The ontogenesis of Fc gamma receptors (FcR) and C3b/C4b receptors (CR1) was studied in peripheral nerves from ten fetuses aged from 20 to 38 weeks using immunohistochemical and functional assays. Monoclonal antibodies (mAbs) against FcR and CR1 stained nerve fibers at 10 weeks of gestation and the staining intensity increased during nerve maturation. FcR and CR1 are probably expressed on Schwann cells and are early markers during the development of peripheral nerves. Functional FcR activity was detected in nerve sections before initiation of myelination, which occurs at approximately 18-19 weeks, whereas functional CR1 activity was found in the sections after myelination. Functional CR1 activity may, therefore, be related to myelin. The ontogenesis of FcR and CR1 was also studied on Schwann cells in culture from three fetuses aged 14, 16 and 19 weeks, using immunofluorescence technique with mAbs. The FcR and CR1 are lost on cultured Schwann cells. This suggests that the receptors are not intrinsic to the cells or that Schwann cells require axonal contact for the expression of FcR and CR1.

Antibodies, Monoclonal↗
PubMed1977

Membrane receptor stripping confirms the association between EBV receptors and complement receptors on the surface of human B lymphoma lines.

Complement (C3) receptors, EBV receptors, Fc receptors, membrane IgM and beta2microglobulin (beta 2m) were individually stripped from the surface of human B lymphoma lines. The cells were subsequently tested for their ability to absorb infectious EB virus. Stripping of Fc receptors, IgM and beta2m did not reduce EBV absorption. Stripping of either EBV receptors or C3 receptors eliminated or drastically reduced EBV-absorptive capacity. The results confirm the distinctive association between EBV receptors and C3 receptors on human lymphoma cells.

Burkitt Lymphoma↗
PubMed1976

Surface markers on human B and T-lymphocytes. IX. Two-color immunofluorescence studies on the association between ebv receptors and complement receptors on the surface of lymphoid cell lines.

Receptors for the third component of complement (C3) were demonstrated on the surface of established human lymphoid cell lines by a membrane fluorescence test with FITC- or TRITC-conjugated antibodies against human C3. Two-color fluorescence staining of EBV receptors and C3 receptors showed complete overlapping of green and red fluorescence. Capping of the EBV receptor induced co-capping of the C3 receptor and vice versa. There was neither overlapping nor co-capping when EBV or C3 receptors were examined in relation to Fc receptors, surface IgM or beta2 microglobulin. The kinetic pattern of EBV receptor capping was identical with the pattern of C3 receptor capping but differed from the pattern of IgM capping. These results suggest a close association between EBV and C3 receptors on the human B-lymphocyte.

B-Lymphocytes↗
PubMed1975

Activated guinea-pig C3 and the immune adherence receptor (a complement receptor) on cell membranes.

By treating C3 with purified C1, C4 and C2 in the fluid phase, haemolytically inactive C3 was prepared. This was shown to bind to human erythrocytes by use of radio-labelled (Fab')2 antibody to guinea-pig C3. The activated C3 preparation inhibited immune adherence between EAC43 and human erythrocytes. These findings indicate that the activated C3 attaches to the immune adherence receptor on human erythrocytes. In addition the fluid-phase activated C3 adhered to thymus cells and sheep erythrocytes, whereas EAC43 did not. Thus the immune adherence receptor may be present on so called immune adherence-negative cells, but in insufficient concentration to form rosettes with EAC43.

Animals↗
PubMed1991

Macrophage hydrogen peroxide production and phagocytic function are decreased following phagocytosis mediated by Fc receptors but not complement receptors.

Previous in vivo and in vitro studies have shown that the phagocytosis of IgG-coated erythrocytes results in a depression of macrophage function. The present study compared the effect of phagocytosis mediated by Fc receptors with that mediated by complement receptors. The phagocytosis of IgG-coated erythrocytes by elicited peritoneal macrophages depressed their capacity to produce hydrogen peroxide as well as phagocytic function. Phagocytosis of erythrocytes coated with IgM and complement had neither of these effects. These results implicate the intracellular signaling that results from Fc receptor mediated phagocytosis in the depression of macrophage function that is caused by phagocytosis.

Animals↗
PubMed1981

Induction of complement receptor expression in cell lines derived from human undifferentiated lymphomas. II. Characterization of the induced complement receptors and demonstration of the simultaneous induction of EBV receptor.

We have studied the specificity of complement receptors induced by theophylline in 2 cell lines derived from undifferentiated lymphomas, one of Burkitt's type, and compared it to that of complement receptors in other cell types. Both C3b and C3d receptors were induced. The induced C3b receptor differed from the C3b receptor of mature normal lymphocytes, polymorphonuclear leukocytes and the cells of a nodular lymphoma in 2 respects. Firstly, it bound C3b much less avidly (by a factor of several hundred-fold) and secondly, we were unable to demonstrate C4b binding. EBV receptors were induced at the same time as complement receptors, and permitted the conversion of a greater fraction of cells to EBNA positivity after experimental infection with EBV. The induction of receptors was not associated with a change in the fluidity of the plasma membranes and our data do not favor a different orientation of induced receptors within the membrane as compared to receptors of other cell types--a potential explanation for the different specificities. Our findings are consistent with the possibility that the complement receptors of lymphocyte precursors differ from these of mature lymphocytes.

Binding, Competitive↗
PubMed1979

Augmentation of macrophage complement receptor function in vitro. I. Characterization of the cellular interactions required for the generation of a T-lymphocyte product that enhances macrophage complement receptor function.

The function of complement receptors of mouse peritoneal macrophages was converted in vitro from mediating only attachment of macrophage complement receptor function was achieved by treating freshly explanted macrophages with supernates from cultures containing T lymphocytes and appropriately triggered macrophages. Fc receptor-mediated phagocyctosis by macrophages was required for the production of active supernates, for neither ingestion via the cells' complement receptors nor ingestion via nonimmunologic means was a sufficient stimulus for the macrophages' participation in the generation of supernatant activity. Fc receptor-triggered macrophages interacted by a contact dependent, but histocompatibility independent, mechanism with T lymphocytes, thereby signalling the lymphocytes to elaborate the active product. The possible significance of enhanced macrophage complement receptor function in inflammation, host defense against microbial pathogens, immune complex disease, and neoplasia is discussed.

Animals↗
PubMed1991

Phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages is mediated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) and IFN-gamma activation inhibits complement receptor function and phagocytosis of this bacterium.

We have examined phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages (MDM). Compared with monocytes, MDM exhibit greatly enhanced adherence of M. leprae (6.5 +/- 2-fold increase). MDM adherence of M. leprae is serum dependent and requires heat-labile serum components because heat inactivation of serum reduces adherence by 70 +/- 3%. mAb against C receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) inhibit phagocytosis of M. leprae in fresh nonimmune serum. Single mAb against each receptor inhibit M. leprae adherence by 25 +/- 4% - 33 +/- 6%. Single mAb used in combination against all three receptors inhibit M. leprae adherence by 51 +/- 6%. Most significantly, pairs of mAb used in combination against all three receptors inhibit by 80 +/- 4%. By electron microscopy, MDM ingest all M. leprae that adhere in fresh nonimmune serum. In the presence of mAb against CR1, CR3, and CR4, the percentage of MDM cross-sections that contain intracellular bacteria is reduced 66 +/- 3% and the mean number of bacteria per cross-section is reduced 78 +/- 10%. MDM activated by IFN-gamma exhibit markedly reduced adherence (by light microscopy) and ingestion (by electron microscopy) of M. leprae. MDM in culture for 5 days inhibit M. leprae adherence by 83 +/- 2% and ingestion by 88% when activated for 5 days. Paralleling this, IFN-gamma-activated MDM exhibit markedly reduced C receptor function, reflected by markedly decreased adherence and ingestion of C3b- and C3bi-coated E. Decreased C receptor function by IFN-gamma-activated MDM correlates with decreased surface expression of CR1 but not CR3 or CR4. CR1 expression on MDM in culture for 5 days is reduced by 32 +/- 9% and 75 +/- 3% after IFN-gamma activation for 5 and 2 days, respectively. This study demonstrates that MDM have an enhanced capacity to phagocytize M. leprae, and that in addition to CR1 and CR3, phagocytosis involves CR4, whose expression on MDM is highly maturation-dependent. This study also demonstrates that IFN-gamma activation markedly reduces the capacity of MDM to phagocytize M. leprae, and it provides a molecular mechanism for this phenomenon-decreased C receptor function.

Antibodies, Monoclonal↗
PubMed1988

Effect of beta-receptor stimulation on Kupffer cell complement receptor clearance function.

The clearance function of complement receptors on Kupffer cells is depressed after several forms of experimental injury. In vitro studies have shown that stimulation of beta-receptors on macrophages causes a depression of several aspects of macrophage function. The present study evaluated the possibility that the increase in sympathetic activity associated with injury contributes to the depression of Kupffer cell complement receptor function. Complement receptor function was assessed in rats from the hepatic uptake of rat erythrocytes coated with IgM. Isoproterenol caused a depression of receptor function when infused at a rate of 5.0 and 0.5 micrograms/kg/min for 15 min but not after infusion of 0.05 micrograms/kg/min. Infusion of isoproterenol, norepinephrine, and epinephrine at 0.5 micrograms/kg/min depressed receptor function by 41%, 38%, and 29%, respectively. Beta-receptor blockade with propranolol prevented the depression of receptor function caused by isoproterenol and norepinephrine. Thermal injury depressed receptor function by 65%, and this depression was reduced to 35% by beta-receptor blockade. Therefore, stimulation of beta-receptors on macrophages by increased circulating levels of catecholamines after injury could contribute to the depression of Kupffer cell function caused by injury.

Animals↗
PubMed1976

Complement receptor lymphocytes in the rabbit. II. The effect of immunization on the complement receptor lymphocyte population in the craining lymph node.

In an attempt to determine the effect of immunization on the size and nature of the complement receptor lymphocyte (CRL) and surface immunoglobulin (SIg)-bearing lymphocyte (B cell) populations, rabbits were injected with 1 mg alum-precipitated keyhole limpet hemocyanin and the cells of the draining popliteal lymph nodes were examined at various intervals for these populations. Comparison to unimmunized control lymph nodes revealed that immunization resulted in an approximate doubling of the percentages of both CRL and B cell populations by the peak of the response, while the cell number increased about 7-to 8-fold. Kinetic analysis of the response indicated that the percentages of CRL and B cells increased essentially in parallel beginning within 40 h after immunization. Simultaneous assay of complement receptor (CR) and SIg disclosed that CRL remained a B cell subpopulation throughout the response. To determine whether cell division could account for the increases in total cell number and per cent CRL and B cells, immunized rabbits were given 3H-thymidine in vivo, and the fraction of labeled (dividing) cells was determined by autoradiography. Results of such experiments were consistent with the possibility that the early increase in cell number and the increase in CRL and B cell percentages were a result of trapping and/or homing of lymphocytes migrating from the peripheral blood. A significant amount of lymphocyte division occurred during later stages of the response.

Animals↗