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PubMed1983

C3b receptors on the cell membranes of the stimulated mouse macrophages. An immunohistochemical study.

C3b receptors were visualized on the cell membranes of stimulated mouse peritoneal macrophages (Mø) by the incubation with cross-reacting swine C3 with proof of this latter by FITC- or HRP-conjugated rabbit anti-swine-C3 antibody. The FITC-conjugate produced a granular and spotty fluorescence. In ultrastructure, the HRP-conjugate revealed minute dense areas of reaction product, whose modest numbers were seen in both aldehyde-prefixed and non-prefixed cell samples.

Animals↗
PubMed1982

Enumeration of lymphocyte populations defined by surface markers in the whole blood of patients with Crohn's disease.

The proportions and absolute numbers of different lymphocyte populations were determined using alkaline phosphatase-labelled reagents in the whole peripheral blood of 22 patients with Crohn's disease. Monoclonal mouse anti-T cell antibody (OKT3) was used to identify T cells, polyvalent F(ab')2 anti-human immunoglobulin for B cells, C3b for C3b-receptor bearing cells, and soluble IgG antibody-antigen complexes for Fc(gamma)-receptor bearing cells. Endogenous myeloperoxidase served to distinguish monocytes. Application of this methodology to whole blood avoids the inevitable loss of cells which accompanies separation of mononuclear cells from blood and therefore permits precise enumeration of lymphocyte populations in the circulation. No significant difference from healthy adult controls was observed in any of the lymphocyte subsets tested.

Adult↗
PubMed1987

Effect of neuraminidase on Fc and C3b receptors on rabbit corneal cells infected with herpes simplex virus.

The effect of neuraminidase on Fc receptors (FcR) and C3b receptors (C3bR) was studied in epithelial, stromal and endothelial cells of the rabbit cornea infected with type 1 (HSV-1) and type 2 herpes simplex virus (HSV-2) in vitro. FcR were induced on epithelial, stromal and endothelial cells of the rabbit cornea by both HSV-1 and HSV-2, but their activities were not enhanced by neuraminidase. On the other hand, the treatment of HSV-infected corneal cells with neuraminidase resulted in the enhancement of C3bR activities on epithelial, stromal and endothelial cells infected with HSV-1, and the enhancing effect of neuraminidase was more pronounced on corneal endothelial cells. A similar neuraminidase treatment had no significant effect on C3bR activities on the corneal cells infected with HSV-2.

Animals↗
PubMed1992

Conservation of receptor expression and phagocytic activity of murine macrophages exposed to various ultrasonic regimens in vitro.

Murine peritoneal macrophages insonated in vitro at 37 degrees C were assayed for impairment of adhesion to and spreading on glass coverslips, expressions of Fc gamma and C3b receptors, and phagocytosis. Insonation conditions were typical for exposures by B-mode imaging equipment and approximated the most severe exposures anticipated in use of pulsed Doppler equipment. In no case were the assay results for insonated samples significantly different from those for the sham-exposed controls.

Animals↗
PubMed1982

The localization of glomerular C3b receptor by immunoelectron microscopy.

By an indirect immunoperoxidase technique, rabbit antiserum to solubilized C3b receptor stained the glomeruli in cryostat sections of human kidney. The staining was localized to the glomerular basement membrane zone. Glomeruli in sections of aldehyde-fixed paraffin-embedded tissue did not stain. However, if the sections were pretreated with proteolytic enzymes, the glomeruli were stained by the antiserum as in the cryostat sections. Electron microscopy revealed that the reaction product was located in the cell membrane of the epithelial cells. In some cells the reaction product was also found in vacuoles in the cytoplasm. The basement membrane and endothelial and mesangial cells did not stain.

Basement Membrane↗
PubMed1981

Similarities of C3b receptors in human kidney and spleen.

Receptors for C3b (C3R) in human spleen and kidney were studied using haemadsorption to cryostat sections. The indicator cells, ovine erythrocytes (E) coated with rabbit IgM antibody (A) and human C3b (EAC) adhered strongly to the glomeruli in renal tissue and to the white pulp of spleen. Titration experiments showed that avidity of the two populations of C3R was equal. Activity was independent of Ca++ and Mg++. Periodic acid, formaldehyde, high salt concentrations and trypsin abolished, whereas neuraminidase enhanced the activity. Various temperatures and pHs affected the two populations of C3R similarly. The results obtained indicate that the C3R in spleen and kidney are similar.

Animals↗
PubMed2000

A new apoptotic pathway for the complement factor B-derived fragment Bb.

Apoptosis is involved in both the cellular and humoral immune system destroying tumors. An apoptosis-inducing factor from HL-60 myeloid leukemia cells was obtained, purified, and sequenced. The protein found has been identified as a human complement factor B-derived fragment Bb, although it is known that factor B is able to induce apoptosis in several leukemia cell lines. Monoclonal antibodies against fragment Ba and Bb inhibited the apoptotic activity of factor B. When the purified fragment Bb was used for apoptosis induction, only the anti-Bb antibody inhibited Bb-induced apoptosis, and not the anti-Ba antibody. The apoptosis-inducing activity was found to be enhanced under conditions facilitating the formation of Bb. Blocking TNF/TNFR or FasL/Fas interactions did not interfere with the factor B-induced apoptosis. CD11c (iC3bR) acts as the main subunit of a heterodimer binding to fragment Bb in the apoptosis pathway, and the factor B-derived fragment Bb was found to possess the previously unknown function of inducing apoptosis in leukemic cells through a suicide mechanism of myeloid lineage cells during the differentiation stage.

Antibodies, Monoclonal↗
PubMed2006

Deletion of Lys224 in regulatory domain 4 of Factor H reveals a novel pathomechanism for dense deposit disease (MPGN II).

We report a novel pathomechanism for membranoproliferative glomerulonephritis type II (MPGN II) caused by a mutant Factor H protein expressed in the plasma. Genetic analyses of two patients revealed deletion of a single Lys residue (K224) located within the complement regulatory region in domain 4 of Factor H. This deletion resulted in defective complement control: mutant protein purified from the plasma of patients showed severely reduced cofactor and decay-accelerating activity, as well as reduced binding to the central complement component C3b. However, cell-binding activity of the mutant protein was normal and comparable to wild-type Factor H. The patients are daughters of consanguineous parents. As both patients but also their healthy mother were positive for C3 nephritic factor, the mutant Factor H protein is considered relevant for unrestricted activation of the disease-causing activation of the alternative complement pathway. Replacement of functional Factor H by fresh frozen plasma (10-15 ml/kg/14 days) was well tolerated, prevented so far disease progression in both patients, and is in the long run expected to preserve kidney function.

Amino Acid Sequence↗
PubMed1981

Demonstration of a C1q receptor on the surface of human endothelial cells.

A receptor for C1q on the surface of human endothelial cells has been demonstrated. This receptor is present on the surface of viable cultured endothelial cells derived from human umbilical veins, and C1q binding can also be demonstrated to the endothelial lining cells of human umbilical artery and vein on frozen tissue sections. Receptors for the complement components C3b and C3d were not detected on tissue sections or endothelial cells in suspension. Endothelial cell C1q receptors are discussed in relationship to possible immune complex localization in vivo.

Binding Sites↗
PubMed1985

Enzyme-linked immunoassay to monitor the purification of, and to screen for monoclonal antibodies against, C3b receptor.

An enzyme-linked immunosorbent assay both to screen for monoclonal anti-bodies to the C3b receptor and to monitor its purification was developed. The test requires only purified C3, converted to either the hemolytically no longer active iC3 or C3b. An NP-40 lysate of tonsil cells can be used as a source of CR1 in this test which works best under hypotonic conditions facilitating the interaction of iC3/C3b and CR1. Two monoclonal antibodies to CR1 were produced using this test for the screening of hybridomas. The identity of the molecule recognized by these antibodies with CR1 is demonstrated by immunoprecipitation and Western blot studies, as well as immunofluorescence and immunoperoxidase staining of cells and tissues known to contain CR1. Fractions from lentil-lectin and DEAE-Sephadex columns containing CR1 can be identified using this test.

Antibodies, Monoclonal↗
PubMed1979

C3b receptors in normal human tissues.

Normal human kidney, lung, liver, heart, skin, thymus, spleen, lymph node, pancreas, and choroid plexus were reacted with a C3b-coated particle (fluoresceinated Salmonella typhi) to determine if these tissues contained C3b receptor cells. Clusters of these cells were identified in the spleen, lymph nodes, and in the renal glomeruli. All other studied tissues demonstrated a minimal homogeneous deposition of the indicator bacteria throughout the entire aspect of the tissue. Deposition of the indicator bacteria on the tissues was abrogated when the bacteria were prepared with heat inactivated serum as a source of complement.

Adolescent↗
PubMed1986

Serotypic variations among virulent pneumococci in deposition and degradation of covalently bound C3b: implications for phagocytosis and antibody production.

To assess serotypic variability in resistance to phagocytosis and in elicitation of antibody response among virulent pneumococci, we quantitated covalently bound C3b and analyzed the C3b degradation fragments for log-phase pneumococci of serotypes 3, 4, 6A, and 14 after opsonization for 20 and 90 min. In C3/C4-deficient agammaglobulinemic serum reconstituted with [3H]C3, covalent binding ranged from 2.9 X 10(4) to 1.5 X 10(5) C3b molecules per organism and increased at least two-fold in the presence of type-specific anticapsular antibody. We compared amide- and ester-linked forms of covalently bound C3b among unencapsulated and encapsulated isolates and differentiated cell wall from capsular binding. Analysis of proteolytic degradation of C3b, covalently bound at the capsular level, revealed C3b, iC3b, and C3d on the capsular surfaces of serotypes 3 and 4, whereas serotypes 6A and 14 displayed only iC3b. We conclude that pneumococcal serotypes, differing in their capsular polysaccharide, differ as well in the amount and site of covalently bound C3b and in its degradative processing to iC3b and C3d. We describe how these differences may explain the well-recognized patterns of serotypic variance in resistance to phagocytosis and in stimulation of antibody production.

Antibodies, Bacterial↗
PubMed1985

Granulocyte and lymphocyte membrane receptors in aseptic meningitis, infectious mononucleosis and other viral infections.

Granulocytes and lymphocytes from 44 patients with acute viral infections were examined for membrane receptors for sheep erythrocytes (E-R), for the Fc portion of IgG (Fc gamma-R) and for complement component C3b (C3b-R). Aseptic meningitis was associated with a decrease in Fc gamma-R and C3b-R bearing granulocytes but an increase in the proportions of lymphocytes bearing the same receptors. Patients with infectious mononucleosis (IM) had a decreased percentage of C3b-R bearing granulocytes, an increase of E-R bearing T lymphocytes and a slight decrease in the proportion of Fc gamma-R and C3b-R bearing lymphocytes. Cerebrospinal fluid from IM patients contained 92-98% T lymphocytes. The group of patients with other viral infections showed a decreased percentage of granulocytes bearing Fc gamma-R and C3b-R, and of E-R bearing lymphocytes. The decrease of Fc gamma-R and C3b-R bearing granulocytes in viral infections may be of importance in relation to the increased risk of bacterial superinfection in these patients.

Cell Membrane↗
PubMed1978

Isolation of various canine leucocytes and their characterization by surface marker analysis.

Various techniques were used to separate canine peripheral blood leucocytes into populations enriched in lymphocytes, polymorphonuclear leucocytes, phagocytic mononuclear cells (monocytes) and macrophages. Surface markers on each cell population were determined by rosette formation. Fc receptors for IgG and complement receptors (C3b and C3d) were present on PMN, monocytes, macrophages as well as on a sub-population of lymphocytes. Purification of the lymphocytes into T-and B-cell-enriched populations revealed that these receptors were present only on the B lymphocytes and not on the T lymphocytes. In addition, a third lymphocyte population, which did not possess surface immunoglobulin, and Fc receptor but not the complement receptor. None of the cell populations exhibited C4 complement receptors or Fc receptors for IgM. When different cell populations were tested for their ability to form rosettes directly with human type 'O' red blood cells it was found that most populations could rosette, suggesting that this technique could not be used as a specific marker for canine T lymphocytes.

Animals↗
PubMed1986

Increased immunoglobulin-secreting cells in the blood of patients with active idiopathic IgA nephropathy.

Peripheral blood lymphocytes from 33 patients with idiopathic IgA nephropathy (IgAN) and 15 healthy controls were stimulated in vitro by Protein A from Staphylococcus Cowan I; immunoglobulin (Ig) production was measured by a reverse hemolytic plaque assay to evaluate the quantity of cells secreting Ig. In addition, serum Ig levels, circulating IgG, IgA and IgM immune complexes (ICs) and the Fc and C3b receptor mediated phagocytosis of peripheral monocytes were measured. The laboratory findings in different phases of the disease were compared. The mean level of IgA-plaque forming cells (IgA PFC) in IgAN patients with normal renal function was significantly higher (p less than 0.001) than the mean control value. In contrast, they were reduced significantly in those patients who were subjected to periodic hemodialysis (p less than 0.001). Disease activity produced a significant increase in IgG PFC and IgA PFC, high IgG and IgM serum levels, high circulating IgG ICs, and low C3b-mediated phagocytic function of the peripheral macrophages. These findings demonstrate that IgAN is associated with an increased number of IgG and IgA-secreting cells in the peripheral blood of patients during the active phase of the disease and that the concurrent presence of high levels of circulating Ig ICs may be responsible for the gross hematuria, as their deposition in the glomeruli could activate the complement system.

Adolescent↗
PubMed1991

Tumor necrosis factor and endotoxin can cause neutrophil activation through separate pathways.

We investigated the possibility that tumor necrosis factor (TNF) mediates neutrophil activation by endotoxin. The number of C3b receptors on the neutrophil cell-surface was used as the indicator of activation, as assessed by indirect immunofluorescence. Incubation of buffy-coat neutrophils with TNF-alpha for 30 minutes at 37 degrees C caused neutrophil activation, increasing C3b receptor-dependent fluorescence from 340 with buffer alone to 580 with TNF (250 pg/mL). Increasing amounts of anti-TNF IgG progressively inhibited neutrophil activation by TNF (250 pg/mL). Addition of the active dose range of anti-TNF to neutrophils incubating in endotoxin (10 ng/mL) did not affect the degree of endotoxin-mediated neutrophil activation. Mixtures of neutrophils with the 50% suppressive dose of anti-TNF and varying endotoxin concentrations showed the same degree of neutrophil activation as mixtures without the antibody. Thus, an antibody that can inhibit TNF-mediated neutrophil activation does not inhibit endotoxin-mediated neutrophil activation. We conclude that endotoxin and TNF can activate neutrophils through separate pathways.

Antibodies↗
PubMed1998

Characterization of C3dg binding to a recess formed between short consensus repeats 1 and 2 of complement receptor type 2 (CR2; CD21).

To allow for a better characterization of the ligand binding structures of human complement receptor type 2 (CR2; CD21), we have established an IgG1 kappa mouse mAb, FE8, that interferes efficiently with binding of C3dg and EBV to CR2. In contrast to mAb OKB7, the only well-characterized mAb with similar specificity, mAb FE8 blocked binding of soluble C3dg or particles carrying multiple copies of surface-bound C3dg to CR2 or induced complete removal of these ligands from the receptor. In vitro EBV infection of B lymphocytes, on the other hand, was abrogated by mAbs FE8 and OKB7 with similar dose-response characteristics. As FE8 was shown to recognize a discontinuous epitope, a series of overlapping peptides derived from SCR1 and -2 and immobilized on cellulose was screened with FE8. The results suggest that up to five discontinuous sequences contributed to the epitope. The sequence 63-EYFNKYS-69, located between the two SCR units, reacted most intensively. Two other sequences, 16-YYSTPI-21 and 105-NGNKSVWCQANN-116, are located between Cys1 and Cys2 of SCR1 and around Cys3 of SCR2, respectively. Based on the solution structure for two factor H SCRs, a three-dimensional model of SCR1 and -2 was generated. The FE8 binding peptide sequences were located in relative proximity to each other, bounding the recess formed between SCR1 and -2. This potential of mAb FE8 is currently unique and may be exploited for interfering with conditions of unwanted recognition of C3dg-coated structures by the immune system.

Amino Acid Sequence↗
PubMed1985

gp140, a C3b-binding membrane component of lymphocytes, is the B cell C3dg/C3d receptor (CR2) and is distinct from the neutrophil C3dg receptor (CR4).

gp140, previously identified as a 140-kDa C3b-binding membrane glycoprotein present on Raji cell surface, was shown to be the C3dg/C3d receptor of B lymphocytes (CR2). Specific polyclonal anti-gp140, prepared by immunizing rabbits with this highly purified C3 receptor, blocked Raji cell rosettes with EC3b, EC3bi, EC3dg and EC3d, and also blocked normal lymphocyte rosettes with EC3dg and EC3d without affecting CR1 or CR3 activity. Moreover, a monoclonal anti-C3 (C3b/#130), described by others as reacting with the d region highly expressed on EC3bi, EC3dg and EC3d and poorly exposed on EC3b, completely inhibited EC3bi, EC3dg and EC3d rosettes with Raji cells, but had no effect on EC3b rosettes. Treatment of Raji cells with rabbit anti-gp140 blocked the uptake of three 125I-labeled monoclonal antibodies anti-B2, HB-5 and OKB7 reported to react with C3d-binding proteins, indicating that each of these monoclonal antibodies recognizes epitopes present on gp140. The neutrophil C3dg receptor was examined to determine its relationship to lymphocyte CR2. While neutrophil rosettes with EC3d were undetectable, a specificity for C3d was suggested by the inhibition of EC3dg rosettes by fluid phase C3d-complexes bearing no detectable C3dg. However, such neutrophil EC3dg and EC3bi rosettes were not inhibited by rabbit anti-gp140 nor an excess of anti-CR1, anti-CR2, and anti-CR3. In addition, neutrophils did not bind 125I-labeled anti-gp140, anti-B2, or HB-5. Thus, the neutrophil C3dg receptor is distinct from gp140, the lymphocyte CR2, and should be designated CR4.

Antibodies, Monoclonal↗