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PubMed2004

Reduced erythrocyte complement receptor type 1 in systemic lupus erythematosus is related to a disease activity index and not to the presence or severity of renal disease.

The present study investigated the expression of the complement receptor type 1 (CR1) on the membrane of erythrocytes (CR1/E) of patients with systemic lupus erythematosus (SLE) by flow cytometry. We found a significant reduction in CR1/E numbers in SLE patients (n = 52), compared to controls (512 +/- 171 and 689 +/- 146, respectively, P = 0.0001). Reduction was more pronounced in active disease patients. The mean CR1/E number observed in patients with inactive disease was 546 +/- 163 CR1/E, while active SLE patients presented a mean of 385 +/- 133 CR1/E (P = 0.001). Patients with SLE with similar activity indexes tend to have similar CR1/E numbers, irrespective of disease severity. We also observed a trend to CR1/E reduction in severe nephritis patients. A small group of SLE patients with chronic renal failure and inactive disease showed CR1/E numbers nearly identical to controls (689 +/- 146 versus 686 +/- 123, respectively, P = 0.95). This was the only group of SLE patients with normal CR1/E numbers. These results confirm the CR1/E reduction in SLE patients as previously described, and also suggest that this reduction is related to disease activity and not to disease severity.

Adolescent↗
PubMed1991

[Activity of erythrocyte complement receptors class 1 in various kidney diseases].

UNLABELLED: The activity of the erythrocyte complement receptors type 1 (CR1) was measured in four groups: a control group--42 healthy persons, 18 patients with lupus nephritis (morphologic types: membranous, membranoproliferative, and proliferative), 16 patients with primary idiopathic membranous glomerulonephritis (GN), 20 patients with primary idiopathic membranoproliferative GN, and 23 chronic haemodialysis patients, in 20 of them the cause of the end-stage renal failure was primary idiopathic GN. The erythrocyte CR1 activity was determined by the immune adherence test. In the groups of the lupus nephritis and of the end-stage renal failure was observed a significant drop in erythrocyte CR1 activity. On the contrary the patients with primary idiopathic membranous and membranoproliferative GN exhibited a significantly greater erythrocyte CR1 activity than the normals. CONCLUSIONS: 1. The genetic predisposition to primary idiopathic GN is not reflected on the level of the erythrocyte CR1 system, what is distinct from the situation occurred in lupus nephritis, despite similarities in their immunopathogenesis. 2. The development of the end-stage renal failure in the course of primary idiopathic GN shows a inhibitory effect on erythrocyte CR1 activity.

Adolescent↗
PubMed1999

Reduction of myocardial infarct size with sCR1sLe(x), an alternatively glycosylated form of human soluble complement receptor type 1 (sCR1), possessing sialyl Lewis x.

1 This study investigated the effects of soluble complement receptor type 1 (sCR1) or sCR1sLex, agents which function as a complement inhibitor or as a combined complement inhibitor and selectin adhesion molecule antagonist, respectively, on the infarct size and cardiac troponin T (cTnT) release caused by regional myocardial ischaemia and reperfusion in the rat. 2 Eighty-two, male Wistar rats were subjected to 30 min occlusion of the left anterior descending coronary artery (LAD) followed by 2 h of reperfusion. Haemodynamic parameters were continuously recorded and at the end of the experiments infarct size (with p-nitro-blue tetrazolium) and cTnT release were determined. 3 Infusion of sCR1 (1, 5 or 15 mg kg-1, each n=7) or sCR1sLe(x) (1, 5 or 15 mg kg-1, n=7, 13 or 13, respectively) 5 min prior to LAD-reperfusion caused a reduction in infarct size from 59+/-2% (PBS - control, n=12) to 46+/-6%, 25+/-9% and 37+/-6% or 42+/-6%, 35+/-6% and 35+/-4%, respectively. 4 Infusion of sCR1 (15 mg kg-1, n=5) or sCR1sLe(x) (15 mg kg-1, n=5) also reduces the myocardial TnT release from 80+/-20 ng ml-1 (control) to 13+/-7 or 4+/-1 ng ml-1, respectively. 5 Thus, sCR1 or sCRsLe(x) significantly reduce infarct size and cardiac TnT release caused by 30 min of regional myocardial ischaemia and 2 h of reperfusion in the rat. The mechanisms of the cardioprotective effects of sCR1 or sCR1sLe(x) are not entirely clear, but may be due complement inhibition and/or prevention of the adhesion and activation of neutrophils.

Animals↗
PubMedDate not supplied

The binding of immune complexes by the erythrocyte complement receptor 1 (CR1).

Immune complexes, which have reacted with complement and bear C3b fragments, bind to the complement receptor 1 (CR1) on human erythrocytes. Indeed, CR1 on erythrocyte serves as a transport system for immune complexes in the circulation so as to prevent immune complex deposition outside the fixed macrophage system. A defect in this transport system has been described in several diseases, in which either complement levels or CR1 number on erythrocytes are diminished. Recent studies have shown that the binding of immune complexes to erythrocytes is favored by the multiple C3b binding sites per receptor and the clustered distribution of CR1 on the erythrocyte surface. Only a few immune complexes bind per erythrocyte but these complexes are tightly bound. The other main function of CR1 on erythrocytes is to enhance the inactivation of C3b by factor I present in plasma. This reaction allows the release of immune complexes from the erythrocyte surface and their transfer to fixed macrophages.

Animals↗
PubMed1996

The N-formyl methionyl peptide, formyl-methionyl-leucyl phenylalanine (fMLF) increases the lateral diffusion of complement receptor 1 (CR1/CD35) in human neutrophils; a causative role for oxidative metabolites?

The effects of the N-formyl methionyl peptide, formyl-methionyl-leucyl phenylalanine (fMLF) on the lateral mobility of the complement receptor type 1 (CR1/CD35) in glass-adherent human neutrophils were investigated, using fluorescence recovery after photobleaching (FRAP) and confocal microscopy (CSLM). It was found that addition of 0.1-1 microM fMLF increased the diffusion constant (D) of CR1/CD35 to 167-228% of controls. No effect was observed on the receptor distribution or the mobile fraction of receptors. The effect of fMLF on the lateral diffusion of CR1/CD35 could be totally inhibited by addition of pertussis toxon (PD, 250 ng/ml) or of the free radical scavenger enzymes superoxide dismutase (SOD, 2000 U/ml) and catalase (CAT, 200 U/ml), added together the results show that oxidative metabolites produced by neutrophils in response to fMLF can modulate CR1/CD35 diffusion, and indicate a regulatory role for oxygen radicals in phagocytosis.

Catalase↗
PubMed1996

Neutralization of Knops system antibodies using soluble complement receptor 1.

BACKGROUND: Antibodies of the Knops system have been referred to as nonneutralizable because they cannot be inhibited with serum, saliva, or urine. Because the Knops system antigens have been located on complement receptor 1 (CR1), the question of whether the antibodies could be neutralized with soluble CR1 (sCR1) produced by recombinant DNA techniques was studied. STUDY DESIGN AND METHODS: First, radiolabeled immunoprecipitation techniques were used to test sCR1 for the expression of the high-incidence Knops system antigens. Then, a total of 45 antibodies were neutralized with sCR1, including the following: one each of anti-Cr(a), -Dr(a), -Do(b), -Hy, -Ge, -Jr(a), -Sc1, -Jk(a), -Cs(a), and -Kp(b); two each of anti-Lu(b), -Yt(a), and -JMH; three each of anti-McC(a), -Rg, and -Sl(a); and four each of anti-Ch, -Kn(a), -Yk(a), -Kn/McC. In addition, two examples of anti-Kn(a) + K, one example of anti-Sl(a) + K + Fy(a), and one example of anti-Yk(a) + E were tested. The sCR1 was added to each test serum and 6-percent albumin was added to the control; this was followed by neutralization incubation for 5 minutes at 25 degrees C. The antibody samples were then tested by a low-ionic-strength solution, anti-human globulin technique. RESULTS: The sCR1 expressed Kn(a), McC(a), Sl,a and Yk(a). All Knops system antibodies (n = 22) were neutralized by the sCR1, but none of the other 23 alloantibodies decreased in reactivity. The samples containing antibodies of two specificities showed inhibition of the Knops system antibody but not of the second antibody. CONCLUSION: This neutralization method, in which recombinant protein is used, provides an expedient and definitive method of identifying Knops system antibodies.

Antibody Affinity↗
PubMed1989

Exacerbation of murine listeriosis by a monoclonal antibody specific for the type 3 complement receptor of myelomonocytic cells. Absence of monocytes at infective foci allows Listeria to multiply in nonphagocytic cells.

Treatment of mice with a rat mAb (5C6) specific for an epitope of the type 3 complement receptor of myelomonocytic cells severely interfered with the ability of the mice to resist infection with Listeria monocytogenes. Consequently, a sublethal infection was rapidly converted to a lethal one that resulted in death in 5 d. However, infection was only exacerbated if 5C6 was given earlier in infection, before mononuclear phagocytes populated sites of Listeria implantation in the liver and spleen. If given after day 3 of infection, 5C6 caused only a temporary increase in bacterial multiplication. The infection-enhancing effect of 5C6 was associated with failure of mice to focus mononuclear phagocytes at sites of bacterial multiplication of Listeria in liver hepatocytes and extracellulary in the spleen. This resulted in unrestricted multiplication of Listeria in hepatocytes and extracellularly in the spleen. The results are in keeping with the ability of 5C6 to inhibit the accumulation of myelomonocytic cells in peritoneal inflammatory exudates, as revealed by a previous study.

Animals↗
PubMed1997

Expression in insect cells of the functional domain of CD21 (complement receptor type two) as a truncated soluble molecule using a baculovirus vector.

We have made use of the plasmid vector pBSV-8His recently established for baculovirus-mediated expression of His-tagged proteins for the production of a truncated soluble complement regulator protein. The protein comprised the N-terminal part, i.e. short consensus repeats (SCRs) 1-4, of the B-cell membrane protein complement receptor type two (CR2; CD21) and contained the functional epitopes which mediate the binding of the complement component C3 fragments C3dg and iC3b. This recombinant protein, termed rsCR2.1-4, was furnished with a C-terminal histidine-tag for easy purification from insect cell supernatant. The yield of > 90% pure rsCR2.1-4 was 3 micrograms/ml supernatant at day eight p.i. RsCR2.1-4 was expressed as two proteins with a M(r) of 29 and 31 representing differentially glycosylated forms. Both reacted specifically with anti-CR2 mAb HB5 directed against SCRs 3-4, but not with anti-CR2 mAbs recognizing SCRs beyond SCR 4. RsCR2.1-4 was able to bind C3dg and to block binding of C3dg-coated beads to Raji cells. Used as antigen for immunization, it allowed the efficient and well-aimed generation of antisera which specifically blocked attachment of C3dg-coated beads to Raji B cells. Thus, insect cell derived rsCR2.1-4 has proved a valuable tool to study the functional domain of CR2 and its immunoregulatory capacity in B-lymphocytes.

Animals↗
PubMed1989

The role of hypocomplementaemia and low erythrocyte complement receptor type 1 numbers in determining abnormal immune complex clearance in humans.

Defective clearance of immune complexes (IC) may contribute to the pathogenesis of diseases such as SLE. We studied the effect of hypocomplementaemia and the influence of erythrocyte complement receptor type 1 (CR1, CD35) number on the clearance of radiolabelled tetanus toxoid (TT)-anti-TT IC from the circulation. These were injected intravenously into 9 normal subjects and 15 patients with diseases characterized by IC formation and/or hypocomplementemia, including 2 with hereditary complement deficiency. IC were found to bind to erythrocyte CR1 in a complement-dependent manner and their degree of uptake was directly correlated with CR1 numbers. Two phases of IC clearance were identified. The first was rapid, occurring within 1 min. Since this phase might represent inappropriate deposition of IC in target organs we called it trapping. It was seen predominantly in subjects with low CR1, low complement, and low binding of complexes to red cells. The second phase was monoexponential with a mean elimination rate of 14.1%/min; it was inversely correlated with CR1 numbers and binding of complexes to red cells. In a second study each individual was injected with IC bound to autologous erythrocytes in vitro using normal serum so that the effects of complement deficiency were eliminated. Up to 81.4% of these bound IC were released in vivo from erythrocytes in 1 min, and the proportion was inversely correlated with CR1 numbers. Only five patients showed trapping, and these had low CR1 numbers and high percentage release of IC. The second phase of elimination was inversely correlated with CR1 numbers and the proportion of IC remaining bound to red cells at 1 min. The two complement-deficient patients had normal CR1: when IC were injected, trapping and very fast clearance rates were observed; however complexes that had been opsonized and bound to erythrocytes were cleared at a slower rate without evidence for trapping. These studies show that complement and erythrocyte CR1 may determine the physiological clearance of certain types of IC and suggest that this system may function abnormally when CR1 number or complement function are reduced.

Antigen-Antibody Complex↗
PubMed1995

Triggering of complement receptors CR1 (CD35) and CR3 (CD11b/CD18) induces nuclear translocation of NF-kappa B (p50/p65) in human monocytes and enhances viral replication in HIV-infected monocytic cells.

Monocyte/macrophages may harbor HIV in a nonproductive fashion for prolonged periods of time. Viral gene expression may be reactivated by stimulation of the cells with LPS or cytokines such as TNF-alpha in vitro. The effect of LPS and TNF-alpha is mediated by their ability to induce nuclear translocation of the DNA-binding heterodimer NF-kappa B (p50/p65), which binds to a specific sequence in the HIV-long terminal repeat. The present study demonstrates that triggering of complement receptors CR1 (CD35) and CR3 (CD11b/CD18) enhances viral replication in HIV-infected human monocytic cells. Monocytic cell lines and normal peripheral blood monocytes were infected with HIV-1 in vitro and cultured in the presence or absence of F(ab')2 fragments of monoclonal anti-CR1 or anti-CR3 Abs or with C3 fragments. Stimulation of CR1 or CR3 induces a two- to fourfold increase in the amount of cell-associated and released p24 Ag in cell cultures that was equivalent to that observed in control cultures triggered with LPS. We further observed that stimulation of CR1 or CR3 induces the nuclear translocation of NF-kappa B p50/p65 in infected cells. Translocation of NF-kappa B p50/p65 was also observed following stimulation of CR1 or CR3 of uninfected peripheral blood monocytes from HIV-seronegative donors. The amount of protein translocated was similar to that observed when cells were stimulated with rhTNF-alpha. TNF-alpha did not mediate the translocation of NF-kappa B p50/p65 induced by triggering of complement receptors. Taken together, these observations suggest that HIV gene expression may be activated in infected monocytes through interaction of the cells with complement-opsonized particles and that enhanced viral replication is associated with C3 receptor-mediated nuclear translocation of the NF-kappa B complex.

Biological Transport↗
PubMed2001

Basic fibroblast growth factor up-regulates the surface expression of complement receptors on human monocytes.

OBJECTIVE AND DESIGN: To clarify the possible involvement of basic fibroblast growth factor (b-FGF) in inflammation, we examined the effect of b-FGF on the surface expression of complement receptors (CR) on human monocytes in vitro. MATERIALS AND METHODS: Heparinized venous blood was obtained from healthy adult donors. The surface expression of CR on blood monocytes was determined by two-color immunofluorescent staining using flow cytometry and monoclonal antibodies. A standard whole blood lysis technique was used to avoid any in vitro manipulation that would activate monocytes. RESULTS: b-FGF increased the expression of CR3 on monocytes in a dose- and time-dependent manner. The b-FGF concentrations used were up to 100 ng/ml. The values of mean fluorescence intensity (MFI) of CR3 expression on unstimulated monocytes were 12.6+/-1.3 (n = 3), whereas those on b-FGF-stimulated monocytes were 59.2+/-7.1 (n = 3). b-FGF also up-regulated the expression of CR1 on monocytes in a dose- and time-dependent manner. The MFI values of CR1 expression on unstimulated monocytes were 2.5+/-0.1 (n = 3), whereas those on b-FGF-stimulated monocytes were 11.1+/-0.6 (n=3). The magnitude of CR1 expression by monocytes was significantly smaller than that of CR3 expression. The maximal stimulatory effect of b-FGF on monocytes was observed using greater than 25 ng/ml of b-FGF and 90-120 min incubation period. CONCLUSION: b-FGF may participate in the inflammatory process by modulating the CR expression on blood monocytes.

Adult↗
PubMed1996

Effects of complement inhibition with soluble complement receptor-1 on vascular injury and inflammation during renal allograft rejection in the rat.

Complement is both an effector of the humoral immune response and a stimulator of leukocyte activation. To examine the influence of complement on the allograft response, we inhibited complement using recombinant human soluble complement receptor-1 (sCR1; TP10), in an unsensitized model of rat renal allograft rejection. Lewis to DA renal transplant recipients were treated daily with 25 mg/kg sCR1 or saline and sacrificed on days 1 to 5 after transplant. Transplanted organs were examined histologically and immunohistochemically for leukocyte subset markers and for the third component of complement, C3, and membrane attack complex deposition. A second set of recipients was followed from day 5 to day 9 to assess graft survival. sCR1-treated recipients displayed > 90% inhibition of plasma complement activity and a marked reduction in tissue C3 and membrane attack complex deposition. Inactivation of complement reduced the vascular injury such that there was almost complete sparing of vascular damage in day 5 sCR1-treated rats. There was a significant reduction in infiltrating leukocytes by day 5 after transplant, and complement inhibition delayed the time to reach a histologically defined end point of graft survival from 5 days in controls to 9 days in the sCR1-treated group. These results imply that the vascular and cell-mediated injury arises, in part, from complement activation. The partial inhibition of these injuries by sCR1 may have functional implications for strategies to inhibit allograft rejection.

Acute Disease↗
PubMed1999

Mechanism of regulation of complement receptor type 1 transcription by cytosine arabinoside in a pre-erythroid model.

Binding to erythrocyte complement receptor type 1 (CR1) clears immune complexes from blood and tissues, preventing complement-mediated pathological inflammation in disease. Previous work has demonstrated that Ara-C, a cytosine analogue, induces an 11-fold increase in CR1 mRNA expression in K-562 erythroleukaemia cells. In this work we therefore investigated whether the Ara-C/K-562 system could be used as a model for studying the pre-erythroid regulation of CR1. We demonstrated that increased CR1 expression could be induced independently of increased haemoglobin expression. Increases in CR1 mRNA levels produced by Ara-C treatment were not a function of increased stability of the message. However, Ara-C induced a protein synthesis-dependent increase in transcription initiation rate as early as 12h after treatment. Further data suggest that the effect of Ara-C on transcription is not a result of its direct DNA-damaging or DNA polymerase-inhibition activities. Induction of receptor transcription was inhibited by tyrosine kinase (TK) and protein kinase C (PKC) inhibitors. These data suggest that TK, PKC and dCTP-adducted phospholipid signalling pathways may all play a role in the mechanism of Ara-C-induced CR1 transcription.

Butyrates↗
PubMed1997

Surfactant prevents quartz induced down-regulation of complement receptor 1 in human granulocytes.

Quartz is known to induce an inflammatory response in the alveolar space by recruitment of different effector cells. We investigated the interaction between granulocytes and quartz with respect to expression of complement receptor type 1 (CR1) and CR3, with and without the presence of surfactant. Granulocytes from hemolyzed blood were stimulated by N-formyl-methionyl-leucyl-phenylalanine (fMLP), which mobilize the intracellular pool of CR1 to the surface, and the mean fluorescence intensity (MFI) measured by cytofluorometry was 47.4 (46-63.6) (median; interquartile range). Quartz exposure reduced the CR1 expression to 23.2 (22.8-30.6) MFI units (P < 0.01), a porcine surfactant preparation added during quartz exposure abolished the down-regulation completely, 47.7 (43.2-62.3) MFI units (P < 0.001). Similar results were obtained after preincubation of the cells with surfactant followed by quartz exposure. No significant influence on CR1 expression was found by a synthetic lipid mixture, nor was the CR3 expression affected. In conclusion, this study demonstrates that the presence of surfactant inhibits quartz induced down-regulation of CR1 on activated granulocytes.

Adolescent↗
PubMed1975

Identification of complement-receptor lymphocytes (B cells) in lymph nodes and tumor infiltrates.

To monitor the distribution of lymphocyte sub-populations infiltrating tumors, a simplified modification of standard techniques was developed to identify the complement-receptor B lymphocytes in frozen tissue sections. This technique is based on binding of antibody-coated bovine erythrocytes by B lymphocytes in the presence of sub-hemolytic concentrations of mouse complement. B lymphocytes can be identified in frozen tissue sections by adherent sensitized bovine erythrocytes. The specificity of the technique for B lymphocytes was established by 1) absence of spontaneous rosette formation with bovine erythrocytes by human T lymphocytes, 2) specific binding of bovine erythrocyte-antibody-complement complexes to B cell regions of normal lymph nodes and spleen and 3) binding of erythrocyte-antibody-complement to a high proportion of chronic lymphocytic leukemia (a B cell leukemia) lymphocytes. Five transitional carcinomas studied had regions of mononuclear infiltration that were virtually devoid of complement-receptor lymphocytes. The results suggest that lymphocytes infiltrating bladder carcinomas may be predominantly T lymphocytes.

Animals↗
PubMed1977

Complement receptor B lymphocytes in nodular sclerosing Hodgkin's disease.

Infiltrated tissues from nine cases of nodular sclerosing Hodgkin's disease (NSHD) were examined for immunologic cell surface markers. In all nine cases a large population of complement receptor B-lymphocytes were present within the nodular infiltrates. B-lymphocytes were identified in frozen sections by adherence of sheep red blood cells (E) coated with IgM antibody (A) and complement (C) IgMEAC). IgMEAC attached to both small lymphocytes and to Reed-Sternberg cells and their variants. Red cells coated with IgG (IgGEA) attached to histiocytes associated with the internodular fibrous bands and only sparsely with the nodular infiltrates. The population of complement receptor lymphocytes appears to be an integral component of NSHD.

Adult↗
PubMed2005

Complement receptor 1 polymorphisms associated with resistance to severe malaria in Kenya.

BACKGROUND: It has been hypothesized that the African alleles Sl2 and McCb of the Swain-Langley (Sl) and McCoy (McC) blood group antigens of the complement receptor 1 (CR1) may confer a survival advantage in the setting of Plasmodium falciparum malaria, but this has not been demonstrated. METHODS: To test this hypothesis, children in western Kenya with severe malaria-associated anaemia or cerebral malaria were matched to symptomatic uncomplicated malaria controls by age and gender. Swain-Langley and McCoy blood group alleles were determined by restriction fragment length polymorphism and conditional logistic regression was carried out. RESULTS: No significant association was found between the African alleles and severe malaria-associated anaemia. However, children with Sl2/2 genotype were less likely to have cerebral malaria (OR = 0.17, 95% CI 0.04 to 0.72, P = 0.02) than children with Sl1/1. In particular, individuals with Sl2/2 McC(a/b) genotype were less likely to have cerebral malaria (OR = 0.18, 95% CI 0.04 to 0.77, P = 0.02) than individuals with Sl1/1 McC(a/a). CONCLUSION: These results support the hypothesis that the Sl2 allele and, possibly, the McCb allele evolved in the context of malaria transmission and that in certain combinations probably confer a survival advantage on these populations.

Child, Preschool↗