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PubMed1988

Macrophage function in chronic experimental alcoholism. I. Modulation of surface receptors and phagocytosis.

In the present study, we have assessed peritoneal, alveolar and splenic macrophages for expression of Fc and C3b surface receptors and their ability to function in immunophagocytosis. We have also measured their oxidative burst response by the nitroblue tetrazolium dye (NBT) reduction method. Our studies revealed that macrophages harvested from chronic alcoholic rats expressed surface C3b and Fc receptors, with significantly higher surface density than macrophages of litter-mate controls (matched for sex and nutritional calories). However, the ability of macrophages from alcoholic rats to phagocytize through C3b and Fc receptors was significantly impaired. In addition, the ability of peritoneal macrophages from alcoholic animals to ingest non-opsonized Candida albicans and to reduce NBT dye was markedly compromised. Abnormalities of macrophage function may, at least in part, account for an increased susceptibility of alcoholic patients to infection.

Alcoholism↗
PubMed1988

Modulation of Fc and C3b receptor expression on guinea-pig macrophages by lymphokines.

The decrease in Fc-receptor-positive cells that occurred during a 6 h incubation of resident and elicited guinea-pig macrophages was partly abrogated when lymphokines were present in the culture. When the same lymphokine preparations were tested on C3b receptor-expression they preferentially sustained the percentage of C3b rosettes formed by resident rather than elicited macrophages. This lymphokine-induced maintenance of Fc and C3b rosettes by cultured macrophages may have been due to an inhibition of receptor release or an increase in receptor synthesis. Supernatants from cultured macrophages contain shed Fc and C3b receptors which inhibit rosette formation by other macrophages. From the demonstration that culture supernatants from both lymphokine-treated and untreated macrophages significantly inhibited Fc and C3b rosette formation by freshly obtained macrophages it seems that the shedding of Fc and C3b receptors is not modified by lymphokines. The maintenance of Fc and C3b rosettes by lymphokines was inhibited by treatment of the macrophages with cycloheximide, suggesting that the lymphokine effect was due to an increase in synthesis de novo of the Fc and C3b receptors. The lymphokine-inducing antigens, BGG and PPD, and control lymphokine preparations were devoid of receptor modifying activity. The reduction in the percentage of Fc rosettes after 6 h culture appears to be due to a loss of Fc receptors for IgG1. Although lymphokines partly inhibited this effect they could not prevent the loss of these receptors following 24 h culture, unlike their action in augmenting the expression of Fc receptors for IgG2. These findings suggest that a selective enhancement of Fc receptor synthesis by lymphokines may modify the functional activities of macrophages.

Animals↗
PubMed1987

Characterization of the C3 receptor induced by herpes simplex virus type 1 infection of human epidermal, endothelial, and A431 cells.

Herpes simplex virus type 1 (HSV-1) infection induces the appearance of viral analogues of human Fc IgG and C3 receptors on the surface of human cells. The virally induced C3 receptor(s) has been broadly defined as a C3b receptor, but its ligand binding characteristics have not been rigorously defined. In this study, human epidermal cells, A431 cells, and human umbilical vein endothelial cells infected with HSV-1 demonstrated rosetting with sheep erythrocytes (E) coated with IgG (E-IgG) or the complement components C3b (EAC3b) or iC3b (EAC3bi), but not with E-IgM, C4 (EAC14), C3d (EAC3d), or E alone. Rosetting was markedly enhanced by pretreatment of HSV-1-infected cells with neuraminidase. Unlike human C3 receptors, the HSV-1-induced C3 receptor was found to be trypsin resistant. To determine whether HSV-1 induced CR1-like receptors or CR3-like receptors, infected cells were pretreated with EDTA, which is known to inhibit native CR3 function. EDTA failed to prevent rosetting with EAC3bi. Furthermore, blocking studies using monoclonal antibodies against CR1 and CR3 revealed that the anti-CR1 antibody 5C11 consistently blocked EAC3b and EAC3bi rosetting with HSV-1-infected cells in a dose dependent manner, but monoclonal antibodies against CR3 did not. This study indicates that the HSV-1-induced C3 receptor is an analogue of CR1.

Antibodies, Monoclonal↗
PubMed1985

Isolation of follicular dendritic cells from human tonsils and adenoids. III. Analysis of their Fc receptors.

Follicular dendritic cells (FDC), isolated from human tonsils or adenoids, were tested for their capacity to retain monomeric, aggregated or antigen-bound human antibodies in the absence of serum. FDC retain fluorescein-labelled heat-aggregated human immunoglobulins, but not monomeric ones nor fluorescein-labelled F(ab')2 in monomeric or aggregated form. Ultrastructural observations showed that colloidal gold-labelled monomeric, or antigen-bound, antibodies directed against tetanus toxoid are retained by dendrites and membrane infoldings of FDC but are never located in cytoplasmic vesicles. This retention was inhibited by incubating FDC with unlabelled aggregated or antigen-bound antibodies. When gold-labelled anti-tetanus toxoid antibodies were incubated in the presence of protein-A before the contact with FDC, a strong reduction of their retention occurred. This further suggested the presence of Fc receptors on isolated tonsillar FDC. Endocytosis was not observed in isolated FDC, even after prolonged incubation in presence of labelled immune complexes: their Fc receptors are, thus, not related to a phagocytic activity as they are in macrophages. Simultaneous ultrastructural labelling of Fc and C3b receptors with colloidal gold particles of different sizes did not reveal any clear relations between these two receptors on the surface of FDC.

Adenoids↗
PubMed1985

Osmotic stress and the freeze-thaw cycle cause shedding of Fc and C3b receptors by human polymorphonuclear leukocytes.

A major problem in the cryopreservation of human polymorphonuclear leukocytes (PMN) is the loss of phagocytic function in cryopreserved cells. This is not a problem with cryopreserved monocytes. To study the reasons for this difference in detail, PMN and monocytes were either osmotically stressed in hypertonic media or were frozen to various temperatures. Cells were then returned to conditions of physiologic osmolarity and temperature. All cells remained viable. However, the ability of PMN to phagocytize bacteria and to bind sheep erythrocytes (E) opsonized with IgG, C3b, or C3bi decreased sharply after exposure to media of 600 mOsM or greater and after freezing to -1.5 degrees C. In contrast, monocytes were unaffected until a concentration of 1500 mOsM or a freezing temperature of -5 degrees C was exceeded. To determine whether the functional losses of surface receptor activity in PMN resulted from a loss of receptors from the membranes or from inactivation or internalization of receptors, opsonized E were incubated in the supernatants from stressed PMN. On subsequent incubation with healthy PMN, these E made fewer rosettes than control opsonized E. The inhibitory effect of the supernatants on rosetting of IgG-sensitized E could be removed by preincubation with IgG bound to Sepharose 4B. Immunoprecipitation of C3b and C3bi receptors from surface-iodinated, osmotically stressed, and control PMN suggested that about 50% of cell surface complement receptors were lost from the cell surface during osmotic stress. These experiments suggest that receptors for IgG and C3 are extruded from PMN cell membranes as a result of hyperosmotic stress, which is associated with the freeze-thaw cycle. This may be an early event in the functional damage done to PMN during attempts at cryopreservation.

Absorption↗
PubMed1985

Human C5a modulates monocyte Fc and C3 receptor expression.

FcIgG and C3 (CR1 and CR3) receptors are responsible for binding opsonized particles, phagocytosis, and immune adherence reactions by circulating and tissue-fixed mononuclear phagocytes. Alterations in the expression of these receptors may thus significantly influence the function of these cells. Because chemoattractants have been shown to both recruit and modulate the function of monocytes, this study specifically examines the effects of human C5a and N-formyl-methionyl-leucyl-phenyl-alanine (FMLP) on human peripheral blood monocyte FcIgG and C3 receptor expression in vitro. Adherent, elutriator-purified monocytes were incubated with C5a (10(-7) to 10(-10) M) or FMLP (10(-5) to 10(-10) M) for 30 min at 37 degrees C, and FcIgG receptor expression was assessed by rosetting with sheep erythrocytes sensitized with limiting dilutions of IgG. Human C5a caused dose-related increases in Fc rosettes of 28% at 10(-9) M, 63% at 10(-8) M, and 167% at 10(-7) M (p less than 0.01). In contrast, no significant increases in monocyte Fc receptor expression were induced by FMLP. Similar rosetting experiments were performed with sheep erythrocytes opsonized with limiting amounts of human C3b to assess C3b receptor expression on adherent human monocytes stimulated with C5a (10(-7) to 10(-10) M) or FMLP (10(-6) to 10(-9) M) for 30 min at 37 degrees C. Again, human C5a caused dose-related increases in monocyte C3b rosette formation; at 10(-8) M and 10(-7) M concentrations of C5a, these increases equaled 119% and 196%, respectively (p less than 0.05). In these experiments, 10(-6) M FMLP also caused a significant increase of 110% in monocyte C3b rosette formation (p less than 0.05). Modulation of monocyte cell surface receptors by human C5a or FMLP was also examined by measuring cell fluorescence and side scatter by dual channel flow cytometry after staining normal leukocytes in citrated venous blood with receptor-specific monoclonal antibodies. These flow cytometric studies demonstrated that both C5a and FMLP induce dose-related increases in CR1 (C3b receptor) and CR3 (iC3b receptor) expression in both monocytes and neutrophils.(ABSTRACT TRUNCATED AT 400 WORDS)

Complement C5↗
PubMed1985

Coincident change of cellular function and phenotype in the course of a suppressor T cell acute lymphocytic leukaemia.

The phenotypic and functional characteristics of the leukaemic cells from one patient with T suppressor ALL were studied at the time of diagnosis and in relapse. At the time of diagnosis, the phenotype corresponded to the intermediate stage between the cortical and medullary phases of normal thymocyte differentiation with a high proportion of T8+ cells (E-R+, TdT+, C3bR-, T3-, T4-, T6+, T8++, T10+). Functionally, the cells did not respond to mitogens but mediated strong suppressor activity to allogeneic B-cells, as measured in a reversely haemolytic plaque test. Clinically, the patient exhibited the uncommon feature of hypogammaglobulinaemia. Induction therapy led to complete remission, which continued for 12 months. In the relapse, the phenotype remained essentially stable except for a dramatic decrease of the T8+ cell fraction and an increase of the T10+ cell fraction. Functionally, the suppressor activity was completely lost, indicating a close correlation between phenotype and functional activity in this leukaemic cell population.

Adult↗
PubMed1985

Effect of dialysable leukocyte extract on the mononuclear leukocytes in Hodgkin's disease.

Therapy with dialysable leukocyte extract repeated 6 times, had a beneficial effect on the impaired functions of mononuclear leukocytes in Hodgkin's disease. The decreased phagocytosis and chemotaxis of monocytes increased almost to the values of healthy controls. There was no significant change in the C3b receptor activity of the patients' monocytes but their pathologically increased EA rosette formation showed some correction during dialysable leukocyte extract therapy. The number of T cells bearing histamine and IgG Fc receptors was reduced initially and increased during therapy but this effect was only temporary. The results suggest that the stimulating effect of dialysable leukocyte extract on cellular immunity was due partly to the correction of mononuclear phagocyte functions rather than an effect on lymphocyte subpopulations in Hodgkin's disease. The beneficial effect of transfer factor on mononuclear phagocyte function may affect the rate of tumour progression and reduce the number of severe infections in patients with Hodgkin's disease.

Antigen-Antibody Complex↗
PubMed1987

Binding of human IgG to cultured urogenital tumor cells.

Binding of human IgG by the Fc portion of the immunoglobulin molecule was detected on established human tumor cell lines by indirect immunofluorescence microscopy, cytofluorography, quantitative absorption, and rosette formation with the use of antibody-coated erythrocytes. Of the nonlymphoid tumors tested, IgG binding was restricted to the cell membranes of certain prostate and urinary bladder tumor cell lines. Although most cell lines tested shared a common antigenic determinant with monocytes and granulocytes, these cells did not express T- and B-cell antigens, the complement 3b receptor, or bind a monoclonal antibody specific for the Fc receptor expressed on human neutrophils. The facts that IgG binding was present on long-term established tumor lines and was not influenced by in vitro passage provide evidence that these properties are intrinsic to the tumor cells and may play some role in the pathophysiology of these tumors.

Adenocarcinoma↗
PubMed1984

[Current theories of phagocytosis and methodological problems in the study of phagocytosis defects in diabetics].

The process of phagocytosis on bacteria is described: recognition of the bacterium by C3b- and Fc-receptors and possibly lektin-like substances on PMN surfaces; ingestion by an actin-myosin interaction in a local Ca++ gradient; simultaneous activation of a NADPH-oxidase and oxidative attack of the bacterial membrane. Special aspects: opsonization, dependence of the rate of phagocytosis on day-time, conditions of diabetics.

Actins↗
PubMed1983

Cerebrospinal fluid granulocytes in bacterial meningitis have E receptors.

Cerebrospinal fluid (CSF) granulocytes from 4 patients with bacterial meningitis were tested for rosette formation with sheep erythrocytes (E), a standard assay for T lymphocytes. CSF granulocytes from all patients formed E rosettes, although to a varying degree (66, 63, 17 and 2%, respectively). E rosettes could not be demonstrated with granulocytes from peripheral blood from the patient with 66% E-rosette-forming granulocytes in the CSF.

Acute Disease↗
PubMed1983

C3b acceptors on human peripheral blood mononuclear cells; characterization and functional role.

C3b acceptors (C3bAs) of human peripheral blood mononuclear cells (PBMC) reacting with the labile binding site of nascent C3b(C3bx) have been investigated by the immune adherence (IA) test. In non-cellular systems some conventional chemical groups (OH-, NH-2) have been reported to be the target of the covalent binding of C3bx. Thus it should be assumed that every cell can fix C3bx via its labile binding site and C3bAs are barely saturable. Contrary to this expectation, however, normal human PBMC were found to be heterogeneous from this point of view, as 57 +/- 4% of B cells and 21 +/- 2% of Null cells possess C3bAs while T cells do not. C3bAs of human PBMC are saturable and trypsin-sensitive structures. The covalent nature of the C3bx-C3bA interaction has also been proved. Studying the effect of acceptor-bound C3b on the function of other cell-surface structures, the inhibition of the Fc gamma receptor function and the abolishment of the enhancement of pokeweed mitogen-stimulated blastogenesis by immune complexes were found.

Antigen-Antibody Complex↗
PubMed1983

The use of frozen erythrocytes in macrophage studies. 2. Attachment and phagocytosis mediated by the two immunological receptors of the macrophages.

Sheep erythrocytes opsonized with IgG or C3b were frozen in various cryoprotective agents, thawed, and compared to corresponding unfrozen erythrocytes exposed to the cryoprotectants and to unfrozen erythrocytes not exposed to the cryoprotectants (controls) as test particles in macrophage attachment and phagocytosis assays. Fc-receptor-mediated attachment and phagocytosis were not influenced by the use of any cryoprotective agent tested or by freezing the erythrocytes. This was also the case with C3b-receptor-mediated attachment. Phagocytosis via this receptor was negligible in normal macrophages, but tended to be slightly more effective when the test particles had been treated with cryoprotective agents. In vitro stimulation of the macrophages with Escherichia coli endotoxin, however, triggered the capacity to internalize treated and untreated erythrocytes equally.

Animals↗
PubMed1982

Demonstration of Fc and C3b receptors on rat perikarya.

Minced rat brain deprived of cerebellum was dissociated by trituration through stainless steel screen and nylon meshes, then by velocity sedimentation technique free-floating perikarya were separated from cell syncytia and cellular debris. The presence of Fc-receptor and C3b-receptor activities, as well as the absence of membrane-bound immunoglobulin and receptor for sheep blood cells were demonstrated on separated perikarya of the rat brain.

Animals↗
PubMed1983

Complement-dependent inhibition of degradation of soluble immune complexes and immunoglobulin aggregates by thioglycollate-stimulated peritoneal macrophages.

Previous studies have shown that the degradation of soluble immune complexes or aggregates (AIgG) by normal peritoneal macrophages can be enhanced by complement. The enhancement of degradation was shown to be at least in part dependent on the number of C3b molecules bound per complex. The present investigations indicate that the enhanced degradation is not found with thioglycollate-stimulated macrophages, and that at high concentrations of complement, inhibition may even occur. The Fc receptor-mediated degradation of soluble immune complexes and AIgG by stimulated macrophages was at least twice as high as that by normal macrophages. This increase was compatible with the increased number of Fc receptors on the stimulated macrophages. The inhibitory effect of high concentrations of serum, as a complement source, on the degradation of AIgG was dependent on the number of C3b molecules bound per AIgG. Although there was also a two-fold increase in the number of C3b receptor sites on the stimulated macrophages, more than 11 C3b molecules per AIgG40 caused significant inhibition of degradation. This phenomenon may be dependent on shielding of Fc-Fc receptor interaction by varying numbers of C3b molecules per complex.

Animals↗
PubMed1983

Immune adherence and staphylococcus protein A binding of soluble immune complexes produced by complement activation.

Complement has been shown to affect the solubility of antigen-antibody complexes by two mechanisms: in the first, classical pathway dependent, complement inhibits the formation of the immune precipitate; in the second, alternative pathway dependent, complement reacts with a formed precipitate to bring about its solubilization. The biological properties of complement reacted immune complexes (IC) has been assessed by studying their binding to staphylococcus protein A (SPA) and to human erythrocytes. BSA-anti-BSA complement reacted IC bound to human erythrocytes and to SPA. Complexes generated by solubilization of immune precipitates showed greater immune adherence than complexes held in solution by complement, despite their similar size. Complexes held in solution in a factor D depleted human serum bound more efficiently to erythrocytes than complexes formed in normal serum. These experiments demonstrate that complement reacted IC cannot be regarded as biologically inert and that factors affecting complement function may have important effects on the properties of antigen-antibody complexes.

Antigen-Antibody Complex↗