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Results for “Fc receptor”

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At least 19 recordsLinked to original sources
PubMed1979

Histamine-binding receptors and Fc receptors of T lymphocytes in SLE.

The participation of TG cells forming the suppressor T cell population and of histamine-binding cells was determined in the peripheral blood of patients with SLE. Former was considerably diminished in the active phase of the disease, latter was found diminished in both the active and the inactive phase. The results published in this paper support the functional disorder of suppressor T cells in SLE, an assumption based only on sporadic data before.

Female↗
PubMed1977

Immunohistochemical detection of Fc receptor. I. Light microscopic demonstration of Fc receptor by using soluble immune complexes of peroxidase-antiperoxidase immunoglobulin G.

The mouse mesenteric lymph node cells (in the cell suspension and frozen sections) were incubated in the soluble immune complexes of peroxidase-antiperoxidase immunoglobulin G. After being washed, they were reacted with diaminobenzidine tetrahydrochloride. Light microscopically brown-colored granules were observed on the cell surface of a proportion of small lymphocytes. In frozen sections, a proportion of small lymphocytes were stained dark brown on the cell surface. Characterization and control experiments suggest that the binding of peroxidase-antiperoxidase immunoglobulin G to the cell surface is mediated by Fc receptor. Peroxidase-antiperoxidase immunoglobulin G, therefore, can be used as in indicator of Fc receptor.

Animals↗
PubMed1977

Immunohistochemical detection of Fc receptor. II. Electron microscopic demonstration of Fc receptor by using soluble immune complexes of ferritin-antiferritin immunoglobulin G.

The mouse mesenteric lymph node cells were incubated in the soluble immune complexes of ferritin-antiferritin immunoglobulin G at 37 degrees C for 20 min. After being washed, postfixed with OsO4 and dehydrated by degraded ethanol series, the lymph node cells were observed by electron microscope. Apprroximately 15% of the cells (mainly composed of small lymphocytes) bound ferritin particles to the cell surface. The distribution pattern of the binding of ferritin particles (ferritin-antiferritin immunoglobulin G) took the form of discrete patches of irregular distribution interspaced with unlabeled portions. The electron microscopic features of ferritin particles (ferritin-antiferritin immunoglobulin G) attached to the cell surface suggest that a structure of constant conformation (Fc receptor) situated in the cell membrane takes part in the binding of ferritin-antiferritin immunoglobulin G.

Animals↗
PubMed1979

Fc-receptor-bearing macrophages isolated from hypersensitivity and foreign-body granulomas. Delineation of macrophage dynamics, fc receptor density/avidity and specificity.

Foreign-body and delayed hypersensitivity granulomas were induced in mice; and the dynamics of macrophages isolated from dispersed, 1--4-week-old lesions was delineated. The size and histologic complexity of the lesions increased as shown: adjuvant greater than schistosome egg greater than methylated bovine serum albumin greater than bead. Esterase staining, spreading on glass, and the percentage of Fc-receptor--bearing macrophages present in the various granulomas reflected the same gradient. The Fc receptors were examined by rosetting with rabbit-antibody--SRBC complex (EA). Whereas more than 90% of the population of macrophages of the dermal adjuvant granuloma contained undiminished numbers of receptor-bearing macrophages throughout the 4 weeks, the percentage of macrophages that displayed receptors in pulmonary foreign-body (40%) and delayed hypersensitivity granulomas (70%) peaked at 1 week and subsequently declined. The EA rosetting of the foreign-body and delayed hypersensitivity granuloma macrophages was strongly inhibited by monomeric IgG2a-specific and weakly by aggregated IgG2b-specific mouse myeloma proteins. Also, macrophages of the delayed hypersensitivity granulomas rosetted in higher percentages with SRBCs coupled with monomeric IgC2a than with those coupled with aggregated IgG2b myeloma proteins. Macrophages of the foreign-body lesion did not react with aggregated IgG2b--SRBC. Rosetting with monomeric IgG2a--SRBC or aggregated IgG2b--SRBC could not be cross-inhibited by the myeloma proteins. Both the monomeric IgG2a--SRBC and aggregated IgG2b--SRBC complexes were readily phagocytized. Trypsin treatment of the macrophages inhibited rosetting with EA or myeloma-protein--coupled SRBCs. The display of Fc receptors on the granuloma macrophages seems to be related to the etiology of the lesion and the intensity and duration of the inflammatory reaction.

Animals↗
PubMed1976

Ia antigens and Fc receptors.

The function of Fc receptors (FcR) on mouse spleen cells as detected by a sensitive rosetting system using antibody-labeled bovine erythrocytes as indicator cells was shown to be inhibited by anti-Ia antiserum. Furthermore, the Ia specificities of each I-region sublocus (I-1A, I-1B, I-C) seem to be associated with FrR, since FcR function was also inhibited when the blocking anti-Ia antiserum recognized only restricted Ia specificities. Antiserum directed against antigens coded for by the K-end of the major histocompatibility complex did not inhibit FcR function. The function of C3 receptors and Fc receptors on macrophages and Fc-receptor-positive cells in the fetal liver was not inhibited by anti-Ia antiserum. These findings are discussed in view of a possible arrangement of Fc receptors and Ia antigens on the cell membrane.

Animals↗
PubMed1979

Studies on the induction of IgG-Fc receptors and synthesis of IgM in primary and chronically-infected lymphoid (Raji) cells by herpes simplex virus.

The present paper reports on the induction of two cell surface markers on human lymphoid cells following herpes simplex virus (HSV) infection. While both primary and chronic infections of human lymphoid cells led to the induction of receptors for the Fc region of 7S IgG, chronic HSV infection was also characterized by the induction of surface-bound IgM. Surface and intracellular Fc receptors were detected in the human lymphoid cell line, Raji, infected with HSV types 1 and 2. Under optimal conditions with a multiplicity of infection (m.o.i.) of 50 to 100 p.f.u. per cell, this marker was inducible in only about 53% of the infected cells. Kinetic studies revealed the appearance of these receptors at around 5 h following HSV infection and they reached a plateau 16 to 18 h p.i. Interestingly, this Fc receptor expression (i.e. percentage of positive cells) was found to be similar in primary and chronically HSV-infected Raji cells. Both human leukocyte interferon and phosphonoacetic acid (PAA), an inhibitor of herpesvirus DNA polymerase activity, effectively inhibited Fc receptor synthesis during primary HSV-infection and these two agents suppressed its induction in chronically HSV-infected Raji (Raji-HSV) cells. This inhibitory or suppressive effect, particularly of PAA, suggests that this HSV-induced Fc receptor may represent a late virus function in the infected cell. Unlike primary HSV infection, about 80% of the chronically HSV-infected Raji cells were found to express surface-bound IgM. This IgM induction was suppressed by long-term interferon treatment but not with PAA-treatment. Superinfection studies of interferon and PAA-treated Raji-HSV cells indicate that only the former would develop Fc receptors suggesting a protective role of this IgM against superinfection by HSV.

Cell Line↗
PubMed1978

Human peripheral lymphocytes bearing surface immunoglobulin do not have readily detectable Fc receptors.

The question of whether human peripheral B lymphocytes have Fc receptors was examined directly by double-label immunofluorescent techniques utilizing assays for detection of Fc receptors, surface immunoglobulin, and complement receptors. Fc receptors were detected by indirect immunofluorescence after incubation with soluble antigen-antibody complexes. Complement receptors were detected by the binding of fluoresceinated bacteria coated with complement. It was demonstrated that most surface immunoglobulin-bearing, complement-receptor positive lymphocytes did not bind soluble antigen-antibody complexes. Conversely, most cells which readily bound soluble complexes did not have surface immunoglobulin or complement receptors. Therefore, most peripheral B lymphocytes do not have easily detectable Fc receptors and most Fc receptor-bearing lymphocytes do not have B cell markers.

Antigen-Antibody Complex↗
PubMed1978

The demonstration of cells bearing Fc receptors in the metrial gland of the pregnant rat uterus.

Cells obtained by collagenase treatment of metrial gland tissue from rats of day 12, 13, 14 and 15 of pregnancy were examined for the presence of surface membrane receptors for immunoglobulin (Fc receptors). Using an EA rosetting technique in which sheep red blood cells (SRBC) were sensitized with a rabbit anti-SRBC immunoglobulin preparation, Fc receptors were found on a proportion of the cells. The majority of the granulated metrial gland cells were not included in the rosetting cell population, suggesting that they do not possess the type of Fc receptor detected by this method. A comparison was made between results obtained when cells were counted in suspension and those obtained from cell counts on sections of fixed material. Both methods were found to yield similar results.

Animals↗
PubMed1978

Fc receptor bearing 'hairy cells' of leukaemic reticuloendotheliosis bind soluble antigen--antibody complexes and adhere to immobilized complexes, but fail to mediate antibody dependent cellular cytotoxicity.

The majority of hairy cells from three patients with leukaemic reticuloendotheliosis were adherent cells bearing surface immunoglobulin, complement receptors, and Fc receptors. Highly purified populations of malignant hairy cells, which readily bound soluble antigen-antibody complexes in suspension and were able to adhere to immobilized antigen-antibody complexes, were examined for their ability to mediate ADCC. Two patients with greater than 90% FcR positive cells failed to mediate ADCC. When initially examined, a third patient, with fewer malignant cells, demonstrated a less marked impairment of cytolysis. When reexamined at a later date, this patient had an increased number of hairy cells and concomitantly demonstrated more impaired ADCC effector cell activity. Absorption of surface immunoglobulin bearing cells onto plastic surfaces coated with goat anti-human immunoglobulin resulted in a complete depletion of FcR, sIg positive, hairy cells. The remaining nonadherent fraction, containing 5.5% FcR positive, sIg negative cells, was able to mediate ADCC as effectively as the normal controls. These results indicate that although FcR bearing hairy cells readily bind soluble antigen-antibody complexes and adhere to immobilized complexes, they were unable to mediate ADCC.

Adult↗
PubMed1979

Electron microscopy of Fc receptors on human lymphocytes.

The membrane receptor for Fc portions of IgG (FcR) was localized on the cell surface of humans lymphocytes by electron microscopy. The electron microscopic markers for FcR were soluble ferritin 7S anti-ferritin immune complexes prepared in forty times antigen excess than needed at equivalence. Fc receptors on the lymphocytes labelled at 0 degree in the presence of sodium azide were seen as discontinuous patches on the cell surface. In control experiments, no labelling was observed, which included lymphocytes treated with ferritin only or with F(ab')2 immune complexes as well as glutaraldehyde-fixed lymphocytes treated with 7S anti-ferritin immune complexes. The findings are discussed with relation to the widely accepted membrane fluidity model.

Antigen-Antibody Complex↗
PubMed1977

Fc receptors on mouse effector cells mediating natural cytotoxicity against tumor cells.

Mouse effector cells mediating natural cytotoxicity against tumor cells have been previously thought to be lymphocytes that lack any detectable cell surface markers. The present study presents evidence for receptors for the Fc portion of IgG on these cells. By adsorption of cytotoxic spleen cells on monolayers of sheep erythrocytes (E) plus IgG antibodies to sheep erythrocytes (EA), 50 to 96% of the total cytotoxic reactivity could be removed. Parallel adsorption of cells on E monolayers or on EA monolayers coated with protein A, to block the Fc portion of IgG, resulted in little or no depletion of cytotoxic activity. The presence of Fc receptors on the NK cells was confirmed by combining EA rosette formation with velocity sedimentation at unit gravity. Peak cytotoxicity occurred at the same sedimentation velocity as the peak of Fc-positive cells. After EA rosette formation, there was a shift to a higher sedimentation velocity in the Fc-positive cells and in the natural cytotoxic activity. The increase in sedimentation velocity of NK activity that was observed in these experiments indicated that most of the cells had only bound a small number (three or four) of antibody-coated erythrocytes. Together, these data indicate that cells with Fc receptors account for most of the total lytic activity of normal mouse spleen cells.

Animals↗
PubMed1978

Possible role of Fc receptors on cells infected and transformed by herpesvirus: escape from immune cytolysis.

Receptors for the Fc portion of nonimmune immunoglobulin G were demonstrated on B103 rat brain neuroma cells infected with herpes simplex virus type 1 (HSV-1) KOS by a radioimmunoassay using 125I-labeled heat-aggregated Fc fragments. Immune F(ab')2 fragments specific for HSV antigens competed efficiently for Fc binding sites, suggesting that the binding of Fc fragments to infected cells is specific for viral cell-surface antigens. It has been suggested that the binding of immune complexes to Fc receptors on the surfaces of tumor cells in vivo plays a role in protecting these cells from immune destruction. In vitro evidence is presented for the ability of aggregated immunoglobulin G molecules bound to cell-surface Fc receptors to protect both HSV-infected and HSV-transformed cells against complement-dependent and cell-mediated immune lysis.

Animals↗