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PubMed1990

Monocyte subpopulations in human gliomas: expression of Fc and complement receptors and correlation with tumor proliferation.

Cryostat sections of 12 gliomas and of 3 peritumoral brain tissue samples were investigated for mononuclear cell infiltration by immunohistochemistry, concentrating on cells expressing monocyte/macrophage markers. Only low numbers of T cells were detected in the tumors, whereas in average 20%-30% of all cells present in the samples were recognized by various macrophage markers. These cells carried surface epitopes with known function, like Fc-gamma (Fcg) and complement receptors. Microglial cells, in comparison to typical debris laden macrophages, were only recognized by a restricted panel of macrophages markers (anti-Fcg receptors 1, 2, 3, complement receptor CR3, HLA DR, common leucocyte antigen CD45 and the monocyte marker RM3/1). In peritumoral tissue mainly dendritic, microglia-like cells were present, which revealed decreased expression of antigens CD4, RM3/1 and Fcg receptors in comparison to those in gliomas. A significant positive correlation was found between the number of RM3/1 or CR3 (CD11b)-positive cells and the proliferation rate of the tumors as documented by the number of bromodeoxyuridine-positive or Ki-67+ cells.

Antigens, CD↗
PubMed1979

Analysis of complement receptors on B-lymphocytes in human milk.

Experiments were performed on human B-lymphocytes in paired samples of milk and blood from the same patient to determine the numbers and percentages of lymphocytes with complement receptors, utilizing the erythrocyte-antibody-complement (EAC) rosette assay. Studies on nine paired samples show the numbers, as well as the percentages, of complement-reactive cells (CRCs) in milk are significantly lower than in blood. Milk lymphocytes were cultured in media containing serum for a 24 hour period to determine if the observed lower numbers of CRCs in milk were due to saturation of the lymphocyte receptors with free complement, as well as to determine if the culture of the cells in nutrient media might result in the reformation of shed complement receptors. Similarly, peripheral blood lymphocytes were incubated in milk supernatant to determine if free complement or other factors in milk might interfere with the EAC assay. These studies support previous findings from this laboratory that B-lymphocytes in milk represent a subpopulation of cells different from those in peripheral blood. The paucity of B-lymphocytes bearing complement receptors in milk may be due to the following: (1) B-lymphocytes in milk may be plasmablasts and/or antibody-producing plasma cells--both known to lack complement receptors; (2) selective processes operating at the mammary alveolar epithelium allowing transit of certain subclasses of maternal immunoglobulins may also allow transepithelial passage of B-lymphocytes with surface immunoglobulins, but no complement receptors. These possibilities are currently being studied.

Antibodies↗
PubMed1989

Antibody to the murine type 3 complement receptor inhibits T lymphocyte-dependent recruitment of myelomonocytic cells in vivo.

We have used the delayed-type hypersensitivity (DTH) response to SRBC or tuberculin to examine the role of the murine type 3 complement receptor in T lymphocyte-dependent inflammatory recruitment. Intravenous injection of 5C6, a CR3-specific rat mAb known to impair myelomonocytic adhesion, divided the DTH to SRBC in actively immunized mice into two phases. The early phase, which lasted 24 h, was characterized by maximal oedema and maximal inflammatory recruitment and was 5C6 inhibitable. The later phase was 5C6 resistant and reached a peak 48 h after antigenic challenge and was superimposable on the declining peak seen in control mice. Passive transfer of reactive T cells mixed with antigen was used to examine the myelomonocytic effector arm of the DTH alone. Both passive transfer of cutaneous DTH to SRBC and passive transfer of the largely monocytic T cell-dependent recruitment to tuberculin in the peritoneal cavity were completely abolished by systemic 5C6 treatment. Injection of 5C6-treated donor leukocytes at the site of passive transfer had no effect. Treatment of donor mice with 5C6 at the time of active immunization did not alter their ability to provide reactive T cells for passive transfer. The myelomonocyte-restricted rat mAb 7/4 and the rapidly cleared F(ab')2 fragment of 5C6 showed no inhibition of the DTH. In all cases, inhibition of footpad swelling correlated with histological evidence of inhibition of myelomonocytic cell recruitment. Peritoneal cell counts after local DTH to tuberculin showed complete inhibition of monocyte recruitment. We conclude that CR3 plays a quantitatively important role in T cell-dependent inflammatory recruitment. This is absolute in passive transfer experiments, but only partial after active immunization. Leukocyte CR3 plays a common role in both immunologically specific and nonspecific inflammatory recruitment and provides a target that could possibly be manipulated to therapeutic advantage.

Animals↗
PubMed1981

Phagocytosis and binding via complement receptors by salivary polymorphonuclear leukocytes. Modulation by saliva and gingival exudate.

The ability of oral polymorphonuclear leukocytes (PMNs) to phagocytose Candida albicans cells and bind Salmonella typhi via complement receptors was investigated. A significantly higher percent of oral PMNs could phagocytose and bind via complement receptors as compared to peripheral blood PMNs. While treatment of peripheral blood PMNs with the donor's saliva caused an increase in the number of complement-receptor bearing cells, as well as a partial increase in phagocytosis, PMNs treated with gingival crevicular fluid (CF) showed a decrease both in phagocytosis and binding. The complexity of environmental conditions and factors, and its role in PMN functions in inflammatory sites is discussed.

Candida albicans↗
PubMed1993

Enhanced eosinophil luminol-dependent chemiluminescence and complement receptor expression by platelet-activating factor and interleukin-5.

The cytokine interleukin-5 (IL-5) and the lipid mediator platelet-activating factor (PAF) have both been shown to be involved in eosinophil differentiation and activation. We have measured and compared the effect of PAF and IL-5 on human eosinophils in terms of their luminol-dependent chemiluminescence (CL) response and their expression of complement receptors, CR1 and CR3. Both IL-5 and PAF enhanced the eosinophil CL response. The optimal concentrations were 40 U/ml for IL-5, and 10(-6) M for PAF. The priming effect of IL-5 was slow and reached a maximal response after 90 minutes incubation. In contrast, the effect of PAF peaked early and declined during incubation. In the complement receptor study, only PAF was able to enhance CR3 expression (p < 0.05) while the effect of IL-5 on eosinophil complement receptor expression was negligible. These results provide evidence that both inflammatory mediator (PAF) and cytokine (IL-5) can activate eosinophils but the effects of IL-5 and PAF on eosinophil CL response appear to be distinct. The activation of eosinophils by PAF and IL-5 may occur through different mechanisms.

Asthma↗
PubMed1988

Lymphocytes expressing type 3 complement receptors proliferate in response to interleukin 2 and are the precursors of lymphokine-activated killer cells.

In the absence of antigenic or mitogenic stimulation, certain peripheral blood lymphocytes exhibit proliferative and lymphokine-activated killer (LAK) cell activities when cultured with recombinant IL-2. Both activities were found to be an exclusive property of lymphocytes expressing type 3 complement receptors (CR3) identified by anti-CD11 monoclonal antibodies. CD11+ lymphocytes were then fractionated into three subsets by two-color flow cytometry. These included CD16+ cells, which display distinctive Fc receptors for IgG (CD16). Using anti-CD5, the CD11+ CD16- lymphocytes were separated into non-T cell and T cell subsets. The two non-T cell subsets (CD11+ CD16+ and CD11+ CD16- CD5-), but not the T cell subset (CD11+ CD16- CD5+), could proliferate in response to IL-2. Both CD11+ non-T cell subsets, but not the CD11+ T cell subset, had the capacity to mediate natural killer cell activity. However, all three CD11+ lymphocyte subsets were capable of generating LAK activity. These findings are consistent with the concept that two signals are required to stimulate T cells to proliferate. However, at least a small subset of blood T cells can be activated by IL-2 to become LAK cells.

Antigens, Differentiation↗
PubMed1988

The clearance of tetanus toxoid/anti-tetanus toxoid immune complexes from the circulation of humans. Complement- and erythrocyte complement receptor 1-dependent mechanisms.

The role of complement and its receptor on erythrocytes (CR1) in the physiologic elimination of large immune complexes from the circulation of humans was assessed. Large radiolabeled soluble tetanus toxoid- anti-tetanus toxoid complexes were injected i.v. into three normal individuals and three patients with SLE. These complexes were prepared in antibody excess and were 45S in size, fixed C and bound to E CR1 in vitro. The percentage of complexes bound in vitro was directly proportional to CR1 number/E in four normal subjects and three SLE patients. After i.v. injection into normal subjects, complexes were cleared rapidly, with a monoexponential rate constant (10.3 to 11% complexes cleared/min). In the SLE patients, clearance was best explained by two phases: the first occurred within the first minute indicating immediate trapping of a fraction of the complexes (19.5 to 25.3% of injected complexes trapped), the second was monoexponential and was similar to the normal range. A large fraction of complexes bound within the first minute to E in vivo; the percentage of binding was variable, ranging from 16.3% to 71.5% and was related to E CR1 number. In a second study complexes were injected that had been attached to autologous E by opsonization with C in vitro. Their elimination was similarly monoexponential, except in one SLE patient in whom there was significant initial trapping (30.9%). A fraction of these complexes were released from E within the first minute, the percentage release being greatest in the patient with the lowest CR1 number (81.4%). E bearing immune complexes remained in the circulation and were not transiently sequestered in the liver or spleen. This is the first study of the clearance of soluble immune complexes in vivo in humans and shows that C and CR1 on E participate in immune complex clearance reactions, and that abnormal clearance can be detected in the form of rapid removal of immune complexes from the circulation.

Adult↗
PubMed1994

Erythropoietin therapy in humans increases erythrocyte expression of complement receptor type 1 (CD35).

The expression of complement receptor Type 1 (CR1, CD35) on erythrocytes (E) is unique to humans and other primates. E-CR1, a C3b/C4b receptor that also acts as cofactor for Factor I, appears to be important in clearing C3/C4-opsonized immune complexes from the circulation, in controlling complement activation in the circulation, and in regulating antibody formation. This study was undertaken to determine whether therapy with recombinant human erythropoietin (rEPO) might increase E-CR1 expression in humans. The rationale is that young erythrocytes express more E-CR1 than old erythrocytes. Thus, conditions that stimulate erythropoiesis should increase E-CR1 expression. The hypothesis that stimulating erythropoiesis by rEPO therapy can increase E-CR1 expression was tested in six anemic chronic hemodialysis (ESRD) patients and five systemic lupus erythematosus (SLE) patients without renal failure. Before the rEPO therapy, three of the SLE patients were anemic and two were not. The ESRD patients were studied before and during 9 or 10 mo of rEPO therapy. The SLE patients were studied before, during, and after 7 mo of rEPO given by sc injection two or three times weekly. It was found that rEPO therapy was associated with a progressive increase in the average number of CR1/E in each of the ESRD patients and in the anemic SLE patients: mean baseline CR1/E was 210 +/- 50 (SE) for the ESRD patients and 125 +/- 35 for the SLE patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Quantification of complement receptor 1 on erythrocytes: follow-up of HIV-1-infected patients with AIDS-related complex/Walter-Reed 5 under treatment with intravenous immunoglobulin. The ARC-IVIG Study Group.

A sensitive flow-cytometric method was established to quantify the number of complement receptor 1 (CR1, C3b/C4b receptor, CD35) on the surface of purified erythrocytes of 12 patients infected by HIV-1 and showing two clinical AIDS-related complex/Walter-Reed 5 criteria. Erythrocytes were incubated with biotinylated monoclonal anti-CR1 antibody followed by phycoerythrin-streptavidin before analysis on a flow cytometer. As few as 50 binding sites/cell could be detected, making this method as sensitive as a radioimmunoassay with 125I anti-CR1. Seven of the patients studied received an immunoglobulin preparation suitable for intravenous use during the 6 months of the study, 5 got an equal amount of placebo preparation consisting of human serum albumin. For a year, erythrocytes were collected and purified every 3 months, frozen and stored at -70 degrees C until the end of the study, when the number of CR1 was determined. No difference between the two groups of patients was found. In 8 patients, small fluctuations of the amount of CR1/erythrocyte were seen during the period of observation, whereas in 4 of the patients a drop of the number of CR1 was observed towards the end of the study. No correlation was found between CR1 numbers on erythrocytes and circulating immune complexes, CH50, C3 and C4 concentrations or CD4-positive lymphocytes.

AIDS-Related Complex↗
PubMed1990

Difference in the clustering of complement receptor type 1 (CR1) on polymorphonuclear leukocytes and erythrocytes: effect on immune adherence.

Complement receptor type 1 (CR1) mediates the adherence of complement-reacted immune complexes (IC) to various blood cells. On the erythrocyte, CR1 are clustered, a distribution which favors efficient multivalent binding of C3b-coated IC. IC can also bind to CR1 expressed on polymorphonuclear (PMN) leukocytes. To evaluate the respective importance of these two cell types in immune adherence reactions, functional analysis of IC binding, as well as morphological studies of CR1 distribution at their surface were undertaken. At equal cell concentrations, resting PMN leukocytes bound the same percentage of IC as erythrocytes, despite expressing four times more CR1 at their surface. At equal CR1 concentrations, IC binding to resting or formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated PMN leukocytes was always lower than to erythrocytes. The morphological counterpart of these differences was studied by label-fracture immunoelectron microscopy. On erythrocytes, almost 50% of the CR1 were distributed in clusters of greater than or equal to 3 units, while less than 15% were grouped in such clusters on the surface of PMN leukocytes. Activation of PMN leukocytes by fMLP increased the surface density of CR1, but the proportion of clustered CR1 remained unchanged. These observations suggest that the low responsiveness of PMN leukocytes towards C3b-coated IC may be due to the unaggregated state of CR1. In the circulation, erythrocytes might function as a "buffer" for PMN leukocytes, which would otherwise engage too swiftly in reactions with IC.

Antigen-Antibody Complex↗
PubMed2001

Localization of Knops system antigens in the long homologous repeats of complement receptor 1.

BACKGROUND: The Sl(a) (Knops system) located on complement receptor 1 (CR1) has been associated with malarial rosetting, a process associated with severe malarial infections. Moreover, the long homologous repeats (LHRs) B and C of CR1 were implicated in rosette formation. As a step toward mapping the location of Knops system antigens, truncated CR1 proteins have been expressed and their ability to inhibit antibodies to the high-incidence Knops system antigens was assessed. STUDY DESIGN AND METHODS: Individual LHRs (A, B, C, and D) of CR1 of the common CR1*1 (F) allotype were expressed as secreted forms in 293T cells. Their abilities to specifically neutralize Knops system antibodies were tested by both hemagglutination and flow cytometry. RESULTS: Three examples of anti-Kn(a) (n = 6) were almost completely inhibited by LHR-C and three by LHR-D. Two examples of anti-McC(a) (n = 2) and seven examples of anti-Sl(a) (n = 8) were inhibited by LHR-D. Both examples of anti-Yk(a) (n = 2) were partially inhibited by LHR-D. CONCLUSION: The high-incidence Knops system antigens reside within LHR-D and to a lesser extent within LHR-C. Because of the role of Sl(a) antigen in malaria rosetting, these results indicate that LHR-D may represent an additional malaria interaction region in CR1.

Antibodies, Monoclonal↗
PubMed2005

B cells from mice prematurely expressing human complement receptor type 2 are unresponsive to T-dependent antigens.

Complement receptor type 2 (CR2/CD21), in association with CD19, plays an important role in enhancing mature B cell responses to opsonized Ags. We have shown that mice expressing a human CR2/CD21 (hCR2/CD21) transgene during the CD43(+)/CD25(-) late pro-B cell stage of B cell development demonstrate marked changes in subsequent B cell ontogeny. In the present study, we show that the humoral immune response to the T cell-dependent Ag, sheep RBC, is muted severely in a manner inversely proportional to B cell expression level of hCR2. Individual Ag-specific IgG isotypes vary in the degree to which they are affected but all are reduced while IgM titers are normal. A substantial reduction in germinal centers, both in size and frequency, in the spleens of immunized hCR2 transgenic mice demonstrates a failure to maintain germinal center reaction. However, both IgM expression levels and LPS-proliferative responses appear fully intact in B cells from hCR2-positive mice, suggesting that this alteration in B cell phenotype is different qualitatively from that of specific Ag-defined anergy models. These data suggest that the unresponsiveness to T-dependent Ags displayed by hCR2-positive B cells is linked to an increase in the level of stimulus required to propel the B cell into a fully activated state and thus a normal humoral immune response to Ags. We conclude that this phenotype and these mice may offer an additional means to dissect mechanisms underlying B cell tolerance and Ag responsiveness both in bone marrow and periphery.

Animals↗
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↗
PubMed1995

Transforming growth factor beta modulates C3 and factor B biosynthesis and complement receptor 3 expression in cultured human monocytes.

Complement biosynthesis in monocytes is stimulated by different pathogens and modulated by a variety of cytokines, but little is known about the possible effect of transforming growth factor beta (TGF-beta) on this monocyte function. We therefore studied the effect of TGF-beta 1 and TGF-beta 2 on constitutive, lipopolysaccharide (LPS)- and Candida albicans-induced monocyte biosynthesis of complement components C3 and factor B. Under all three conditions, both forms of TGF-beta (20 ng/ml) induced a two- to fourfold increase in C3 concentration in monocyte supernatants harvested after 2 or 5 days of cell culture, an effect that was abrogated by cycloheximide. In contrast, constitutive and pathogen-induced production of factor B was suppressed by TGF-beta. The effects of TGF-beta on complement production were neutralized by a monoclonal anti-TGF-beta antibody. Moreover, TGF-beta suppressed the pathogen-induced release of granulocyte-macrophage colony-stimulating factor and down-regulated the expression of complement receptor 3 (CD11b/CD18), while the expression of CD11a/CD18, a related beta 2 integrin, was unaffected. These novel effects of TGF-beta emphasize the immunomodulatory significance of this cytokine.

Adjuvants, Immunologic↗
PubMed1991

Elimination of soluble 123I-labeled aggregates of IgG in patients with systemic lupus erythematosus. Effect of serum IgG and numbers of erythrocyte complement receptor type 1.

Using soluble 123I-labeled aggregates of human IgG (123I-AHIgG) as a probe, we examined the function of the mononuclear phagocyte system in 22 patients with systemic lupus erythematosus (SLE) and 12 healthy controls. In SLE patients, a decreased number of erythrocyte complement receptor type 1 was associated with less binding of 123I-AHIgG to erythrocytes and a faster initial rate of elimination of 123I-AHIgG (mean +/- SEM half-maximal clearance time 5.23 +/- 0.2 minutes, versus 6.58 +/- 0.2 minutes in the controls), with possible spillover of the material outside the mononuclear phagocyte system of the liver and spleen. However, multiple regression analysis showed that serum concentrations of IgG were the most important factor predicting the rate of 123I-AHIgG elimination. IgG concentration may thus reflect immune complex clearance, which in turn, would influence the inflammatory reaction, in SLE.

Adolescent↗
PubMed1976

The glomerular complement receptor in immunologically mediated renal glomerular injury.

We examined 25 renal-biopsy specimens to determine whether there is a relation between immunologically mediated renal diseases and the activity of complement receptors that selectively bind antigen-antibody complexes containing activated third component of complement (C3b). These receptors have been termed glomerular complement receptors. Renal lesions associated with in vivo deposition were associated with a loss of receptor sites as demonstrated by reduced or absent in vitro binding of C3b-coated test reagents by glomerular complement receptor. These findings suggest that binding of complement containing immune complexes to glomerular complement receptors in human subjects may participate in the immunopathologic processes of certain immune-complex-mediated renal diseases.

Antibody Specificity↗
PubMed1997

Characterization of complement receptor type 1 and type 3 mRNA expression on polymorphonuclear leucocytes (neutrophils) in gingival crevicular fluid from periodontitis-affected patients.

A previous study has demonstrated that complement receptors on the surface of polymorphonuclear leucocytes (neutrophils) in gingival crevicular fluid significantly increased compared with those in autologous peripheral blood obtained from periodontitis-affected subjects. The present study attempted to determine the mRNA levels of complement receptor types 1 and 3 (CR1, CR3) on neutrophils in gingival crevicular fluid using reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. Gingival crevicular fluid samples were obtained from 11 adult periodontitis patients by gingival crevicular washing, and venipunctured peripheral blood was used as a control. RT-PCR analysis was performed using the primer sets for CR1, CR3 and beta-actin. Digoxigenin-labelled RNA probes were synthesized from RT-PCR products for in situ hybridization. Both CR1 and CR3 mRNA levels relative to beta-actin were significantly lower in crevicular fluid neutrophils than in peripheral blood neutrophils (crevicular fluid-CR1, 32.75 +/- 22.93%, peripheral blood-CR1; 65.30 +/- 43.25%, p < 0.005; crevicular fluid-CR3; 9.09 +/- 5.34%, peripheral blood-CR3; 30.14 +/- 18.80%, p < 0.005). In in situ hybridization, a greater majority of neutrophils showed positive CR1 and CR3 mRNA expression, while only a few neutrophils showed positive signals in gingival crevicular fluid. Data in the present study suggest that increased expression of complement receptors on the neutrophil cell surface appears to be unrelated to de novo synthesis.

Female↗
PubMed1994

Neutrophils from patients with myelodysplastic syndromes: relationship between impairment of granular contents, complement receptors, functional activities and disease status.

Myelodysplastic syndromes (MDS) are stem cell disorders of clonal origin in which infections and leukemic transformation are quite frequent. Neutrophils from 28 patients with MDS were analysed by flow cytometry for the expression of the two complement receptors CR1 and CR3, the antigenic reactivity of some granule constituents--myeloperoxidase, lysozyme, elastase, lactoferrin--and functional activities, such as locomotion, respiratory burst and cytotoxicity. The results were correlated with the FAB disease subtypes, grouped as low risk (RA) and high risk patients (RAEB, RAEB-t, CMML) and with 30 healthy subjects. A significant reduction in the percentage of neutrophil CR1, CR3 positivity and chemotaxis induced by endotoxin-activated serum was detected in the high risk group when compared with the low risk group and healthy controls. Furthermore, the high risk group also showed a low amount of myeloperoxidase, elastase, lysozyme and superoxide anion, but both low and high risk groups displayed reduced cellular cytotoxicity in comparison with the control. This work indicates that MDS patients belonging to the more advanced FAB categories frequently show multiple abnormalities in the expression of neutrophil complement receptors, and granular components (> 3), as well as in cell functions, suggesting the possibility of using these phenotypic abnormalities in the monitoring of disease progression.

Chemotaxis, Leukocyte↗