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PubMed1990

The leukocyte cell surface receptor(s) for the iC3b product of complement.

CR3 is probably the major adhesion molecule on monocytes and neutrophils. Its function as a phagocytic receptor for iC3b-coated particles has been well characterized. CR3 also has binding affinity for other ligands, including those that compete with iC3b such as fibrinogen, factor X, and beta-glucan, and those that do not such as bacterial LPS. CR3 binding to endothelial cells probably plays an important role in the extravascular migration of monocytes and neutrophils, but the ligand that it recognizes on endothelial cells has not been identified. Structurally CR3 belongs to the integrin family, and it shares a common subunit with p150,95 and LFA-1. The expression of these three membrane antigens appear to be limited to leukocytes, and they are sometimes referred to collectively as the leukocyte integrins. All three antigens have a common binding affinity for bacterial LPS. p150,95 also has affinity for iC3b, but p150,95/iC3b-dependent cellular responses has not been demonstrated. Its status as a complement receptor therefore awaits further experimental support.

Amino Acid Sequence↗
PubMed1986

Effects of inflammation products on immune systems. Lysophosphatidylcholine stimulates macrophages.

Microbial infection causes inflammation which stimulates macrophage functions. One of the inflammatory products, lysophosphatidylcholine (lyso-Pc), can stimulate macrophage activities. Treatment of mice with lyso-Pc enhanced spreading and ingestion activities of peritoneal macrophages. In vitro treatment of macrophages with lyso-Pc greatly enhanced spreading but not ingestion activities. However, incubation of a mixture of adherent and nonadherent cells with lyso-Pc produced a markedly enhanced ingestion activity of macrophages, implying the contribution of nonadherent cells to the stimulation of macrophages. Time course studies of the stimulation of these macrophages showed that spreading activity is stimulated immediately, even 30 min, after their contact with lyso-Pc while induction of ingestion activity requires a latent period of about 5 h. When the specificity of the macrophage receptors for ingestion was analyzed using defined immunoglobulins (i.e., IgG and IgM) with or without complement, lyso-Pc-activated macrophages efficiently ingested IgG-coated sheep erythrocytes independent of complement. However, macrophages of the same lyso-Pc-treated mice did not ingest erythrocytes coated with IgM and complement. These observations suggest that lyso-Pc-stimulated macrophages ingest the targets via Fc-receptors but not C3b receptors.

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↗
PubMed1984

Factors influencing immune complex localisation.

In systemic immune complex (IC) diseases such as SLE and rheumatoid vasculitis, IC accumulate in a number of tissues, either after deposition from the circulation or from in situ formation. The tissue localisation of IC depends on a delicate balance between the production of IC and the ability of the mononuclear phagocytic system (MPS) to remove them from blood. At times IC are cleared inefficiently, persist in the circulation and subsequently localise in tissues. This review evaluates the role of local tissue factors - anatomical, physiological, physical and immunological - in this process. We report on our studies examining the significance of C3b and IgG Fc receptors in tissues subject to IC deposition. No evidence for such receptors was found with the exception of a C3b receptor in human glomeruli. Our negative findings may be due to methodological difficulties in the identification of in situ receptors. Alternatively, immune receptors may not be present at these extra-glomerular sites and would therefore be unlikely to participate in IC localisation.

Animals↗
PubMed1986

In vitro studies on the Fc-receptor function of mononuclear phagocytes in rheumatoid arthritis: relation between the Fc-receptor blockade and the concanavalin A-binding capacity of autologous immunoglobulin G.

The Fc-receptor (Fc-R) function of monocytes isolated from 19 control subjects and from 30 patients presenting with a rheumatoid arthritis (RA) was assessed in vitro by a classical rosette assay using IgG-coated sheep red blood cells. In RA patients, the percentage of monocytes forming rosettes was significantly lower than in controls (34.4 +/- 20.4 versus 67.4 +/- 4.5%; P less than 0.001). The blockade observed was reversed by a prior trypsin treatment of RA monocytes, the percentage of recovery being correlated with the IgG plasma levels. Besides, IgG purified from the serum of four RA patients bound a mean of 7.3, 5.2, 1.6, and 1.6 times more than normal IgG did onto concanavalin A (Con A), peanut agglutinin (PNA), phytohemagglutinin (PHA), and pokeweed mitogen (PWM), respectively. Although similar amounts of 125I-labeled normal and RA IgG were bound to normal monocytes, RA IgG inhibited more efficiently than normal IgG the Fc-R function of normal monocytes, for all concentrations tested (10 to 100 micrograms/100 microliters). A prior treatment of RA IgG by alpha-mannosidase, but not by beta-galactosidase, significantly reduced their inhibitory properties. The incubation of monocytes with D-mannose or mannan reduced their capacity to form rosettes. The percentage of monocytes forming rosettes in the presence of both mannan and normal IgG was significantly lower than that measured in the presence of normal IgG only. On the contrary, the rosetting capacity of monocytes in the presence of both RA IgG and mannan was the same as that calculated in the presence of RA IgG only. The inhibitory effect of RA IgG was not related to their abnormal circular dichroism. Our data suggest that the greater ability of RA IgG to block the Fc-R function of monocytes probably depends on the presence of a greater number of accessible mannosyl residues on the glycosidic side chains located in the Fc domain of the molecules.

Adult↗
PubMed1990

Nonsteroidal antiinflammatory agents inhibit upregulation of CD11b, CD11c, and CD35 in neutrophils stimulated by formyl-methionine-leucine-phenylalanine.

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit PMN aggregation, chemotaxis, degranulation, and superoxide anion production stimulated by synthetic formyl peptides. Many of these functions are dependent upon receptors for the complement components C3b and iC3b (CD35 and CD11b, respectively), or the adherence molecules CD11b and CD11c. Using flow cytometry and specific monoclonal antibodies, we studied the effects of the NSAID piroxicam and indomethacin on the upregulation of these cell surface proteins on PMNs stimulated with FMLP, C5a, or ionomycin. Incubation of PMNs at 37 degrees C increased the expression of all three of these surface proteins. A further increase was induced by stimulation with FMLP, C5a, or ionomycin. Both piroxicam and indomethacin inhibited FMLP-induced upregulation of CD11b, CD11c, and CD35, but neither drug affected the upregulation of these surface molecules induced by C5a or ionomycin. Furthermore, piroxicam had no effect on 37 degrees C-induced upregulation of any of the surface proteins, while indomethacin showed no effect on 37 degrees C-induced CD11b upregulation but suppressed CD11c and CD35 upregulation. Inhibition of surface protein upregulation by FMLP was not due to inhibition of FMLP binding to PMNs. We conclude that piroxicam and indomethacin inhibit FMLP receptor-mediated upregulation of CD11b, CD11c, and CD35 in PMNs, but have no effect on the upregulation of these molecules by ionomycin or C5a. These data suggest that piroxicam and indomethacin interfere with postreceptor signaling events specific to PMN stimulation by FMLP.

Adult↗
PubMed1991

Ratio of complement receptor over Fc-receptor III expression: a sensitive parameter to monitor granulocyte-macrophage colony-stimulating factor effects on neutrophils.

In vitro activation of human granulocytes leads to altered expression of distinct surface antigens. Compared with the changes observed with classic activating reagents such as the phorbol ester PMA similar, but less pronounced alterations of surface antigen expression were observed upon granulocyte activation with human recombinant granulocyte-macrophage colony-stimulating factor (hrGM-CSF). In particular, stimulation with hrGM-CSF is followed by an enhanced expression of the complement receptors CD35 (CR1) and CD11b (CR3) while the low affinity Fc-gamma receptor CD16 (FcRIII) is downregulated. In order to investigate whether there are similar effects under in vivo conditions, we studied the granulocytes from patients undergoing rhGM-CSF therapy before, during, and after treatment. We found a marked increase in CD35 (CR1) and CD11b (CR3) expression and a substantial decrease or even loss of CD16 (FcRIII) on these granulocytes. These changes correlated well with our in vitro data and occurred extremely rapidly after therapy onset. Furthermore, therapy monitoring using ratios calculated by the mean fluorescence channel numbers of CR and FcRIII stainings may combine the advantage of high sensitivity with high reproducibility as a result of the contrasting change in CR and FcRIII expression during granulocyte activation. Being nonparametric values, such ratios are not influenced by individual flow cytometry standardization. Taken together, these activation-associated changes of surface receptor expression and especially of CR over FcRIII ratios are useful parameters for monitoring the in vivo effects of rhGM-CSF.

Antigens, CD↗
PubMed1992

Neutrophil function in whole blood and after purification: changes in receptor expression, oxidase activity and responsiveness to cytokines.

Neutrophil function and plasma membrane receptor expression was measured in cell suspensions isolated by two separate procedures and in unfractionated whole blood. When cells were prepared by a combined dextran/ficoll procedure, their ability to generate reactive oxidants in response to fMet-Leu-Phe was greater than in corresponding cells isolated by a one-step procedure on Mono-Poly Resolving Medium (M-PRM). Cells prepared by both methods could be primed in vitro by rGM-CSF, but the priming ratio was greater in cells prepared by the latter method. The ability of neutrophils in whole blood to generate reactive oxidants in response to fMet-Leu-Phe was extremely low, but this was increased by more than 10 fold if the blood was pre-incubated with rGM-CSF. Similarly, expression of CD 11b and CD 16 was very low (or undetectable) in neutrophils in whole blood, but this was rapidly increased upon priming. Activation by PMA resulted in a down regulation of CD 16 expression as the receptor was shed from the cell surface. Neutrophils isolated by either the dextran/ficoll or the M-PRM method showed increased expression of receptors compared with those in whole blood, although this expression was lower in cells isolated by the latter method. These data indicate that the isolation procedures used to obtain purified neutrophils prime both receptor expression and oxidase function, although these effects are minimalised in isolation procedures using M-PRM. Furthermore, as CD 16 expression on neutrophils in whole blood is rapidly up-regulated during priming, it seems likely that, as for complement receptors, rapidly-mobilisable intracellular stores of this receptor exist.

Antibodies, Monoclonal↗
PubMed1995

Increased expression of complement receptor type 1 (CR1, CD35) on human peripheral blood T lymphocytes after polyclonal activation in vitro.

The receptor for C3b and C4b--complement receptor type 1 (CR1, CD35)--is present on a variety of cell types including erythrocytes, phagocytic cells, B lymphocytes and a small subpopulation of T lymphocytes. The function of the receptor varies according to the different cell types, but on T lymphocytes the function is as yet not known. The present study concerns the influence of polyclonal stimulation on CR1-expressing T lymphocytes. Incubation with PHA resulted in a dose-dependent increase in the number of CR1-positive T lymphocytes. The CR1-expression T lymphocytes were found in both the CD4- and the CD8-positive subpopulation, but a significant stimulatory increase was only found in the CD4-positive population. A significant increase in the number of CR1-expressing T lymphocytes was found when monocytes were present during stimulation, indicating an importance of monocytes and/or monocyte products. However, the increase was not regulated by arachidonic acid metabolites of the cyclo-oxygenase pathway as indomethacin failed to inhibit the increase. Neither did rIL-1 alpha, rIL-1 beta, rTNF alpha nor rIL-6 alter the number of CR1-expressing T lymphocytes. The results of this study indicate a role for CR1 on T lymphocytes in the regulation of the immune system.

Concanavalin A↗
PubMed2005

IgG and complement receptor expression in children treated by peritoneal dialysis.

Children treated by peritoneal dialysis (PD) are at increased risk of infections. IgG receptors (FcgammaRs) and complement receptors (CRs) on white blood cells (WBCs) are important for the phagocytic process. We have investigated FcgammaR and CR expression on monocytes, macrophages and neutrophils in blood and in peritoneal dialysis effluent (PDE) of 39 PD children. WBCs were isolated from blood and PDE, labelled with FITC-conjugated CD16 (FcgammaRIII), CD32 (FcgammaRII), CD64 (FcgammaRI), CD11b (CR3) and CD35 (CR1) monoclonal antibodies, and analysed by flow cytometry. Peritoneal cells had lower percentages of FcgammaR-positive or CR-positive cells than blood. On the other hand, the receptor number per cell [mean fluorescence intensity (MFI)] was higher on peritoneal macrophages and neutrophils than blood, except for CD16. The FcgammaR and CR expression in blood and dialysate did not change significantly during the first year of PD treatment. During a peritonitis episode the MFI of all receptors in blood increased only on monocytes, with the exception of CD32. The percentages of FcgammaR-positive and CR-positive macrophages and neutrophils in the PDE increased, whereas the MFI did not increase consistently. Peritoneal cells of PD children showed a lower percentage of FcgammaR-positive and CR-positive neutrophils and macrophages, combined with an increased MFI, indicating a state of activation. Blood and peritoneal cells are capable of up-regulating the receptor expression during peritonitis but probably not to a maximum level.

Adolescent↗