Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Receptors, Complement 3b”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1984

Granulocyte Fc-IgG and C3b receptor expression in the primary myelodysplastic syndromes (MDS): relationship with dysgranulopoiesis and evidence for heterogeneity of morphological subgroups.

The expression of Fc-IgG and C3b membrane receptors by granulocytes and their precursors was examined in 78 patients with primary myeloid dysplasia (MDS). The marrows were categorized into five morphological groups, broadly corresponding to those described by the FAB group, and further graded into mild and severe according to the severity of dysgranulopoiesis. Fractionated bone marrow and peripheral blood granulocyte receptors were assessed by rosette formation with optimally sensitized ox erythrocytes and the results compared with those found in 17 normal marrows and with those previously reported in megaloblastic anaemia. Fc-IgG and C3b receptor expression was generally increased in maturing granulocytes in all MDS diagnostic groups but premature expression was particularly marked in chronic myelomonocytic leukaemia and refractory cytopenia. Receptor patterns showed a better correlation with the severity of dysgranulopoiesis than with the morphological types. It is suggested that, as in megaloblastic anaemia, changes in membrane receptor expression reflect nuclear-cytoplasmic asynchrony. The results further indicate considerable immunological heterogeneity of granulocytes within individual MDS categories.

Granulocytes↗
PubMed1984

Electrophoretic and cytochemical characterization of alpha-naphthyl acetate esterases in acute myeloid leukemia: relationships with membrane receptor and monocyte-specific antigen expression.

Alpha-naphthyl acetate esterases (ANAE) were examined by cytochemical and isoelectric focusing (IEF) techniques in 48 cases of acute myeloid leukemia that were classified by conventional morphological criteria. Four main types of ANAE isoenzyme patterns were found by IEF, and comparisons with the expression of membrane receptors (Fc-IgG and C3b) and monocyte-specific antigens (UCHM1, UCHALF, and E11) suggest relationships between ANAE isoenzyme synthesis and distinct myeloid maturational stages. The results further indicate that the blast cells of acute myelomonocytic leukemia (AMML) may represent an immature variant of monocytic leukemia (AMoL) and that morphological examination alone is inadequate in the assessment of monocytic differentiation in acute myeloid leukemias. Inhibition studies of cytochemical ANAE activity with sodium fluoride (NaF) show that the presence of NaF-sensitive or NaF-resistant ANAE enzymes is often unrelated to the diagnostic category of acute leukemia. The results of this study are examined in relation to current concepts of myeloid differentiation, and the application of these findings to the subclassification of acute myeloid leukemias is discussed.

Antibodies, Monoclonal↗
PubMed1984

Lymphoblastoid cell supernatants increase expression of C3b receptors on human polymorphonuclear leucocytes: direct binding studies with 125I-C3b.

Human PMN incubated in culture supernatants of the Raji long-term human lymphoblastoid cell line showed increased rosette formation with sheep erythrocytes coated with C3b (EIgM C4b3b) but no change in rosette formation with IgG-coated erythrocytes. This suggested a specific increase in cell surface C3b receptors, which was further investigated using 125I-C3b for direct binding studies. The results confirmed that specific binding of 125I-C3b to PMN incubated in culture supernatants increased up to three- to four-fold over binding to PMN incubated in control media alone. Scatchard analysis revealed that the apparent Ka for supernatant-treated cells, 3.36 +/- 0.89 X 10(7) L/M did not differ from the Ka for cells incubated in control media, 3.76 +/- 0.75 X 10(7) L/M, suggesting an increase in a single class of C3b receptors. Kinetic studies revealed that the active factor was present within 24 hr of culture of the Raji cells, and that neutrophils incubated in culture supernatants increased their C3b receptors continuously for up to 4 hr, the longest interval tested. The effect of the culture supernatant was lost with dilution beyond eight- to 10-fold. The results suggest that culture supernatants of this long-term lymphoblastoid cell line contain soluble factors that induce increased expression of C3b receptors on PMN and may thus serve as a model for study of important physiologic effects of lymphocyte products on PMN in vivo.

Cell Line↗
PubMed1984

Defective binding of the third component of complement (C3) to Streptococcus pneumoniae in multiple myeloma.

Patients with multiple myeloma (MM) are at an increased risk for infections with bacteria that require opsonization with complement. Because Streptococcus pneumoniae is the most frequently encountered pathogen in these patients, we investigated the ability of serum from patients with MM to mediate the binding of C3b, the major opsonin of the complement system, to S. pneumoniae. S. pneumoniae types 3, 14, and 25 were chosen for study, since S. pneumoniae type 3 activates primarily the classical complement pathway (CCP), type 25 primarily the alternative complement pathway (ACP), and type 14 both pathways. S. pneumoniae were treated with normal serum or serum from 17 patients with MM, and the bound C3b was quantified with fluorescein-conjugated anti-C3 in a spectrophotofluorometric assay. Despite normal or elevated serum concentrations of C3, total hemolytic complement, and C-reactive protein in all of the MM sera, factor B in 16/17 such sera, and C4 in 14/17 MM sera studied, all 17 sera demonstrated a defect in C3b binding to type 3 (32.7% +/- 6% of normal). In addition, serum from 15/17 patients bound decreased amounts of C3b to types 14 (39.6% +/- 8%) and 25 (52.2% +/- 8%). Mixing normal serum with MM serum restored MM C3b binding activity to all three S. pneumoniae types, suggesting that the defect was related to a deficiency rather than an inhibitor of C3 activation. Although MM patients are unable to produce specific antibodies to bacterial antigens, the addition of anti-S. pneumoniae antibodies to MM serum did not enhance C3b binding to any of the S. pneumoniae types. However, when S. pneumoniae were opsonized in a mixture of MM serum and C3-depleted normal serum, C3b binding was restored to all three S. pneumoniae types, demonstrating that MM C3 functions normally in the presence of other normal serum factors. In the present studies, the MM C3b binding defect appeared to correlate with the incidence of S. pneumoniae infections. Serum from patients with a history of an S. pneumoniae infection bound significantly less C3 (20.5% +/- 4%) than those study patients without a history of an S. pneumoniae infection (55.8% +/- 8%) (p less than 0.0025). Thus, MM serum has a defect in the activation of C3, and this may contribute to the increased susceptibility of MM patients to S. pneumoniae infections.

Complement C3↗
PubMed1984

Altered surface distribution of both C3b receptors and Fc receptors on neutrophils induced by anti-C3b receptor or aggregated IgG.

Human neutrophils to which monospecific Fab' or F(ab')2 anti-C3b receptor had been bound at 0 degrees C were incubated for timed intervals at temperatures ranging from 0 degrees C to 37 degrees C, after which the cells were labeled with TRITC -conjugated second antibody. Neutrophils bearing Fab' anti-C3b receptor and incubated for up to 30 min at 37 degrees C, and cells bearing F(ab')2 anti-C3b receptor and incubated at 0 degrees C, exhibited diffusely distributed punctate clusters of receptors. Neutrophils bearing the bivalent anti-receptor and incubated at 30 degrees C or 37 degrees C for 5 min had redistributed C3b receptors into caps and patches that were associated with subplasmalemmal accumulations of myosin. The redistribution of cross-linked C3b receptors was inhibited by pretreatment of the neutrophils with either cytochalasin D or chlorpromazine. On approximately one-half of the cells demonstrating capped C3b receptors there was a corresponding redistribution of Fc receptors, as demonstrated by subsequent binding of FITC-aggregated IgG (FITC agg-IgG). In contrast, capping of C3b receptors did not alter the diffuse distribution of HLA-A on these cells. Cross-linking of Fc receptors on neutrophils by FITC agg-IgG also induced temperature-dependent capping of these receptors that was inhibited by cytochalasin D and chlorpromazine. In approximately one-half of the cells demonstrating capped Fc receptors, subsequent labeling of C3b receptors revealed a similar redistribution of these receptors. Thus, the neutrophil responds to cross-linking of either C3b receptors or Fc receptors by a cytoskeletal-dependent rearrangement of both receptors that causes their overlapping topographic distribution, demonstrating a form of cooperative interaction between these two types of receptors that are involved in the phagocytic reactions of these cells.

Animals↗
PubMed1984

Factors influencing the endocytosis of immune complexes.

The MPS plays an important role in the removal of both particulate and soluble immunogenic material from the circulation. E.IgG adhere to mononuclear phagocytes if the Fc portion of the IgG can interact with the phagocyte's Fc receptors (Fc gamma R). Simultaneous sensitization with IgG and C3b via complement activation enhances the effectiveness of binding and ingestion. E.IgM adhere mainly via C3b to C3b receptors (C3bR) of macrophages. Unstimulated macrophages do not ingest E.C3b. Stimulated macrophages, on the other hand, can ingest E.C3b. If soluble material cannot adhere to the surface of macrophages, it will be endocytosed in vitro via fluid-phase pinocytosis at the concentration that is present in the medium. If the material adheres to the cell's surface via its chemical properties or via specific receptors, it will be selectively concentrated at the cell's surface and endocytosed by adsorptive pinocytosis. Ingestion of IC via Fc gamma R and C3b depends on the ability of the antibodies to interact with Fc gamma R and their capacity to activate the complement system. IC-bound C3b enhances the adsorptive pinocytosis of IC. Soluble AIgG are also pinocytosed more effectively when C3b is bound to AIgG. The degree of endocytosis varies with the level of C3b sensitization. The highly effective C3b-mediated pinocytosis can be abolished by treating with trypsin to inactivate C3bR. This observation illustrates that C3b-mediated pinocytosis can replace Fc-mediated pinocytosis in unstimulated macrophages. When macrophages are stimulated in vivo, Fc-mediated pinocytosis increases significantly. Under these conditions, the binding of C3b no longer stimulates; instead, it sterically interferes with Fc-Fc gamma R interaction. In vivo, E.IgG are removed mainly by splenic macrophages. C4-deficient guinea pigs clear E.IgG less effectively than guinea pigs with an intact complement system. On the other hand, soluble IC and AIgG are removed from the circulation mainly by hepatic Kupffer cells. Complement depletion does not seem to influence the clearance rates of these soluble IC or AIgG. The different results obtained in vitro and in vivo and the finding that different effector organs are responsible for the removal of sensitized erythrocytes and soluble Ic in vivo, suggest that more reliable techniques have to be developed to measure IC clearance in patients with a supposedly deficient or saturated MPS.

Animals↗
PubMed1984

Characterization of the inflammatory cells in progressing tumor-like alveolar hydatid cyst. 2. Cell surface receptors, endocytosed immune complexes and lysosomal enzyme content.

Alveolar hydatid cysts (LCM) grow progressively and contribute significantly to the morbidity of hydatid-hosts. To examine whether modifications in immune effector parameters correlate with the pattern of LCM growth, in vivo experiments were carried out in C57BL/6J mice infected intraperitoneally with LCM. Immigrant peritoneal and intra-LCM leukocytes were tested for the loss of cell surface receptors, membrane-bound and internalized immune complexes (ICs) and lysosomal enzyme contents during the restrictive and progressive growth phases of the LCM. The proportion of Fc and C3b receptor-bearing intra-LCM leukocytes decreased 2-fold and 31 to 72% of the leukocytes contained ICs during the progressive phase of the LCM. Acid phosphatase and beta-glucuronidase activities of macrophages declined sharply during the restrictive phase but they gradually increased as the infection progressed. IC-mediated dysfunction of effector leukocytes and modulation of antibody dependent cell cystolysis mechanism are discussed in murine hydatidosis.

Acid Phosphatase↗
PubMed1984

Phagocytosis of immune complexes by human neutrophils and monocytes: relative importance of Fc and C3b receptors.

Human neutrophils and peripheral blood monocytes were studied for their Fc- and C3b-receptors after incubation of the cells with two types of immune complexes (IgG or F(ab')2. Immune complexes can bind to and activate phagocytes via Fc- and C3b-receptors. On mononuclear phagocytes an additional receptor is found that is able to interact directly with F(ab')2-complexes. C3b- and Fc-receptors can mediate ingestion of appropriately opsonized particles, C3b-receptors being at least as efficient as Fc-receptors. The extents of cell activation and phagocytosis in vitro depend on a number of variables, like complex size, ligand (antibody, C3b) density on the surface of opsonized particles, receptor number etc., which are not controlled in most studies and thus may explain the discrepant results reported in the literature. With the in vitro results obtained here, we cannot fully explain in vivo data obtained by various groups, where F(ab')2 antibodies yielded full protection against different types of infections. Therefore, great caution must be applied in all attempts to extrapolate in vitro data to the actual situation in vivo.

Animals↗
PubMed1995

Leukocyte activation in the peripheral blood of patients with cirrhosis of the liver and SIRS. Correlation with serum interleukin-6 levels and organ dysfunction.

OBJECTIVE: Leukocyte adhesion plays an important role in inflammation. Adhesion molecules such as CD11b on polymorphonuclear neutrophil leukocytes (PMNs) up-regulate in response to tumor necrosis factor-alpha, interleukin-8 (IL-8), and other mediators that are involved in systemic inflammatory response syndrome (SIRS). This study examined the behavior of CD11b and other membrane molecules in SIRS in relation to serum cytokines and the severity of illness. DESIGN: Survey study. SETTING: Liver transplantation intensive care unit at a tertiary care center. PATIENTS: A consecutive sample of 22 patients admitted to the liver transplantation intensive care unit for complications related to cirrhosis of the liver in the absence of other disease. Sixteen of the patients developed SIRS and multiple organ dysfunction syndrome with suspected bacterial infections. Seven control subjects were also studied. MAIN OUTCOME MEASURES: Modified Goris organ failure score and Acute Physiology and Chronic Health Evaluation II score. RESULTS: Mean serum IL-6 levels, but not IL-1 beta or tumor necrosis factor-alpha levels, correlated with organ failure (r = 0.79, P < .001). Leukocyte cell-surface markers fluctuated from day to day. The mean of several values was more stable. Mean CD11b and CD35 on PMNs correlated with serum IL-6 level (r = 0.75, P < .001, and r = 0.77, P < .005, respectively). Up-regulation of both CD11b and CD35 display on PMNs correlated with organ failure (r = 0.74, P < .001, and r = 0.71, P < .01, respectively). Polymorphonuclear neutrophil leukocyte L-selectin, CD31, and CD16 were simultaneously decreased, consistent with PMN activation. Monocytes appeared to be activated, but the pattern of surface molecule display was different. CONCLUSIONS: In human SIRS, the circulating monocyte and PMN pools undergo alterations suggestive of leukocyte activation, including up-regulation of PMN CD11b in correlation with the serum IL-6 level and severity of organ dysfunction.

Adult↗
PubMed1994

[Effect of complement type 1 receptor pre-binding on the phagocytosis mediated by Fc receptor].

As a result of IgG-Fc interaction, sheep erythrocytes sensitized with IgG (E-IgG) are constitutively phagocytosed by resting PMN, although in low numbers. The low efficiency of the system can be improved by opsonization with C3b, since the combination of C3b and IgG makes a powerful opsonic signal. It is accepted that the mechanism of C3b enhancement of IgG mediated phagocytosis is achieved by increasing the adherence of the targets to the phagocyte. Recently, a non-opsonic role for C3b enhancement of IgG mediated phagocytosis has been proposed, in cultured human monocytes. These cells, when adhered on glass surfaces precoated with C3b, showed a marked increase in E-IgG internalization. The effect was dose dependent and it was reproduced utilizing a monoclonal antibody against CR1 (C3b receptor). In the present work we studied the existence of this phenomenon in resting neutrophils and in neutrophils stimulated with two kinds of agents: a phorbol ester (PDBu), which activates the CR1 and fMLP, which increases the expression of this receptor. In previous experiments we determined that the adherence of resting neutrophils on different concentrations of iC3 (which binds CR1 and exerts the same effect that C3b), did not increase the phagocytosis of the E-IgG, using as a control neutrophils adhered on the same concentrations of human serum albumin (HSA) (data not shown).(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1994

Tumor necrosis factor induces a block in the cotranslation of Fc gamma RIIb mRNA in mouse peritoneal macrophages.

Macrophage activation results in the secretion of various proteins, such as inflammatory cytokines and proteases. In parallel, cell morphology is altered, and the repertoire of cell surface proteins is modified. One of the main functions of macrophages is phagocytosis via Fc gamma-receptors (Fc gamma R). This study explores the modulation of Fc gamma Rs and their mRNAs following activation of macrophages by tumor necrosis factor. It shows that the cell surface expression of Fc gamma RI and Fc gamma RIIb is strongly reduced in macrophages cultured in the presence of tumor necrosis factor, whereas the mRNA of the Fc gamma RIIb is strongly increased as the result of an increase in mRNA stability. Thus, Fc gamma RIIb expression is modulated during macrophage activation by a new mechanism involving posttranscriptional regulation.

Animals↗
PubMed1994

Modulation of Fc and C3b receptor activity of mouse peritoneal macrophages elicited by preformed immune complexes.

A study was undertaken to reveal the role of Fc and C3b receptor of mouse peritoneal macrophages (MPM) in the uptake of radiolabelled immune complexes. Large latticed preformed complexes consisting of human serum albumin (HSA)-anti HSA at equivalence (IC-Eq) and with antibody excess (IC-Ab) were observed to be avidly taken up by resident macrophages unlike small size complexes with antigen excess (IC-Ag). Macrophages elicited by thioglycollate (Tg) showed higher IC-binding capacity while IC-elicited MPM showed reduction in the same when compared to the resident cells. However, complement coated complexes were significantly taken up by these IC-elicited macrophages. Uptake studies were further extended to determine the expression of Fc and C3b receptor activity in MPM when elicited with preformed IC. Tg-elicited MPM were observed to bind greater number of IgG-coated erythrocytes (E-IgG) than resident MPM whereas IC-elicited MPM bound E-IgG poorly. When Fc receptors were blocked by in vitro IC treatment, poor binding of complement coated E-IgG [E(IgG)C] was recorded in resident MPM. The present complement medicated rosetting data tends to show enhanced expression of C3b receptors on IC-elicited macrophages.

Animals↗
PubMed1994

[Effects of dimethylformamide on the monocytophagocytic system of rodents].

The effects of Dimethylformamide (DMF) on monocytophagocytic system (MPS) of rodents were studied. The results showed large dose of DMF (1/20 LD50) with oral administration could significantly inhibit the functions of colloidal carbon clearance of MPS in Wistar rats, and of non-specific phagocytosis of sheep red blood cells (SRBC) by peritoneal macrophage in Kunming mice, and could also lowered significantly the levels of Fc and C3b receptors on the surface of peritoneal macrophage in mice. This showed DMF could cause obvious damage to MPS.

Animals↗
PubMed1994

In vivo activation of naive T cells by antigen-presenting B cells.

In vivo experiments were performed to determine if the cross-linking of mlg on antigen-presenting B cells could induce them to present Ag to naive T cells in a stimulatory rather than a tolerogenic fashion. Mice were injected with a foreign mAb to a B cell Ag (Fc epsilon RII or CR1), and/or a self-anti-IgD mAb. Injection of either mAb alone failed to induce an Ab response; however, simultaneous injection of the foreign anti-B cell mAb plus the self-anti-IgD mAb stimulated a large response. Inasmuch as injection of the anti-IgD mAb should not have facilitated transfer of the foreign mAb to dendritic cells, this observation suggests that cross-linking of B cell mlg can induce B cells to acquire the ability to present Ag to naive T cells in an activating manner. Furthermore, when injected with anti-IgD mAb, both foreign anti-B cell mAbs were more potent in inducing Ab responses in this system than were isotype-matched control mAbs, consistent with the hypothesis that T cells were activated by Ag-presenting B cells. Results of dose-response and cell transfer studies, however, suggested that stringent cross-linking of B cell mlg on large numbers of B cells is required for B cell Ag presentation to induce T cell activation rather than tolerance. Therefore, these observations suggest that professional APCs usually are required to activate naive T cells, and that B cell Ag presentation can only activate naive T cells under unusual circumstances.

Animals↗
PubMed1996

LPS induces CD14 association with complement receptor type 3, which is reversed by neutrophil adhesion.

CD14, a glycosylphosphatidyl inositol (GPI)-linked membrane protein, is a key membrane binding site for LPS (endotoxin). Although CD14 lacks transmembrane and cytoplasmic sequences, it activates CR3-mediated leukocyte adhesion and cytokine release. Since CR3 has been shown to interact with other GPI-linked membrane proteins, we tested the hypothesis that CD14 can physically associate with CR3. Using qualitative and quantitative resonance energy transfer microscopy, we show that LPS in the presence of serum or LPS binding protein triggers formation of CD14-CR3 complexes. Kinetic studies show that CD14-CR3 complexes dissociate as neutrophils attach to substrates. We speculate that LPS-charged CD14 enhances CR3-mediated adhesion by directly binding to CR3.

Adult↗
PubMed1996

Dehydroepiandrosterone modulation of lipopolysaccharide-stimulated monocyte cytotoxicity.

Dehydroepiandrosterone (DHEA), the predominant androgen secreted by the adrenal cortex, can be converted to both potent androgens and estrogens. In addition to its role as a precursor for other steroid hormones, DHEA has been proposed to play an important role in immunity. This study has investigated DHEA modulation of LPS-induced monocyte cytotoxicity. Cytotoxicity markers assessed include tumor cell killing, IL-1 secretion, reactive oxygen intermediate release, nitric oxide synthetase activity as measured by the release of reactive nitrogen intermediates, complement receptor-1 cell surface protein, and TNF-alpha protein presence. Monocytes stimulated with LPS concentrations of 1.0 micrograms/ml displayed the above cytotoxic markers, whereas monocytes stimulated with DHEA alone or with LPS at a lower concentration of 0.2 ng/ml did not. However, when used simultaneously, DHEA and LPS 0.2 ng/ml displayed a synergistic effect on monocyte cytotoxicity against cancerous cell lines, IL-1 secretion, reactive nitrogen intermediate release, complement receptor-1 cell-surface protein, and TNF-alpha protein to levels comparable with levels obtained using LPS 1.0 microgram/ml. Finally, Scatchard plot analysis demonstrated the presence of a DHEA receptor in monocytes, suggesting that DHEA effects on LPS-stimulated monocytes are mediated through a receptor-dependent process.

Adjuvants, Immunologic↗