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Monocyte functions in patients with mixed connective tissue disease.

The authors investigated the number and functions of peripheral blood monocytes in patients with mixed connective tissue disease. Moderate monocytopenia was detected in the active stage of the disease. There was a close correlation between the sensitized sheep red blood cell binding capacity of monocytes and the elevated levels of circulating immune complexes. The yeast phagocytosis of monocytes and the chemotactic activity were normal in patients with mixed connective tissue disease. C3b receptor mediated phagocytosis of monocytes decreased in the active and inactive stages of the disease. This study suggests that the decreased function of C3b receptors of monocytes is related to the pathogenesis of this disease.

Adolescent↗
PubMed1989

[Study of the relation of the typology of nephrotic syndrome and red cell C3b receptor, T cell function].

This paper reports the determined results of rosette rates of red cell C3b receptor and active rosette (Ea) rates of T lymphocyte in 39 cases of nephrotic syndrome. Typology of nephrotic syndrome according to TCM differentiation symptoms, all the 39 cases were divided into three types: (1) 13 cases of deficiency of Qi of the Spleen with stagnancy of dampness; (2) 9 cases of deficiency of Yang of the Spleen and Kidney; (3) 17 cases of deficiency of Yin of the Liver and Kidney. The results showed that the red cell C3b receptor rosette rate and Ea rosette rate in 39 cases of nephrotic syndrome were significantly lower than those in the control. The difference between the two groups was very obvious (P less than 0.001) among the three types. The rosette rates of both in the deficiency of Qi of the Spleen and deficiency of Yang of the Spleen and Kidney were markedly decreased than those in the control (P less than 0.001). Whereas, the red cell C3b receptor rosette rate was lower than that in the control (P less than 0.01), and T cell Ea rosette rate showed no statistical difference (P greater than 0.05) in the deficiency of Yin of the Liver and Kidney. There was a close relationship between the immune dysfunction of red cell and the pathogenesis in nephrotic syndrome. There was markedly relationship between the pathogenesis of deficiency of Yang of the Spleen and Kidney and deficiency of Qi of Spleen with stagnancy of dampness and T cell immune dysfunction. While the Ea level in deficiency of Yin of the Liver and Kidney was closely correlated with the control. Probably this type was nephrotic nephrosis which had been treated with TCM-WM.

Adolescent↗
PubMed1989

Regulation of human neutrophil type 3 complement receptor (iC3b receptor) expression during phagocytosis of Staphylococcus aureus and Escherichia coli.

Human neutrophils (PMN) express a receptor for iC3b, a cleavage product of C3b. CR3 is an important receptor for phagocytosis of opsonized bacteria and its expression is enhanced by cell activation. We examined PMN CR3 expression during phagocytosis using flow cytometry and a CR3-specific monoclonal antibody. After 30 min phagocytosis of opsonized S. aureus and E. coli, CR3 expression increased to 151% and 221% of controls, respectively. Unopsonized S. aureus had no effect on CR3; however, unopsonized E. coli enhanced CR3 expression despite not being phagocytosed. Time-kinetic studies indicated a rapid initial fall in CR3 after addition of bacteria to PMN, followed by enhanced expression within 5-10 min. The initial fall in CR3 probably represented CR3 internalization rather than receptor destruction, as superoxide dismutase, catalase and protease inhibitors had no effect on this. Correlation of CR3 expression with the PMN oxidative response, measured with the intracellular fluorescent probe DCF-DA, demonstrated a dichotomy. Opsonized S. aureus and E. coli caused an oxidative response from PMN but unopsonized E. coli, which caused significant CR3 up-regulation, did not. CR3 up-regulation with unopsonized and opsonized E. coli was markedly inhibited by Polymyxin B, suggesting a role for endotoxin. These experiments indicate that CR3 expression can be regulated during phagocytosis, and the mechanisms responsible are distinct from those involved in the oxidative burst. CR3 up-regulation following exposure to bacteria in vivo may enhance neutrophil function at sites of infection.

Escherichia coli↗
PubMed1989

Coagulation increases neutrophil CR1 and CR3 expression: primary role for platelet-derived growth factor.

Neutrophil receptors for C3b(CR1) and C3bi(CR3) mediate a number of functions important for infection control and tissue repair, such as adherence, aggregation, orientation in chemotactic gradients, and phagocytosis of opsonized particles. We studied the effect of the coagulation of whole blood on the induction of neutrophil complement receptor (CR) expression in vitro. Neutrophils incubated in serum for 1 hour at 37 degrees C increased the expression of CR1 3.43-fold and CR3 3.06-fold compared with incubation in buffer (p less than 0.001). In contrast, incubation in plasma did not induce such an increase. The serum factor responsible for this CR-inducing effect appeared to be a platelet constituent, because (1) serum derived from platelet-rich plasma, but not platelet-poor plasma, contained the CR-inducing factor; (2) pretreatment with aspirin inhibited the adenosine diphosphate-induced expression of this factor in platelet-rich plasma; (3) the CR-inducing factor was also contained in supernatants derived from frozen/thawed platelets; (4) pure platelet-derived growth factor (PDGF) induced CR expression to the same extent as did whole serum; and (5) the CR-inducing activity of serum and platelet supernatants was inhibited by incubation with antibody against PDGF but not by antibody against C5. Thus, a platelet component that is probably PDGF appears to be the major CR-inducing factor generated during in vitro coagulation and may play a vital role in mediating the neutrophil response to tissue injury and inflammation.

Aspirin↗
PubMed1989

Accelerated nonproteolytic cleavage of C3 in plasma from patients with primary biliary cirrhosis.

Complement 3 (C3) with decreased net charge and altered immunoreactivity was detected by crossed immunoelectrophoresis when EDTA plasma from patients with primary biliary cirrhosis was incubated in vitro after reconstitution with Ca++ and Mg++. The alpha and beta chains of this C3 were intact. C3 with decreased net charge was not detected in patients' fresh plasma. Similar C3 alterations were obtained after reaction between native C3 in serum from healthy persons or purified C3 nucleophiles that induce cleavage of the single thioester bond in the alpha chain of C3. This C3 alteration was unchanged when the reaction occurred in the presence of protease inhibitors. The electrophoretically slow C3 fraction was labile in serum on further proteolytic cleavage of C3. It is suggested that accelerated nonproteolytic C3 cleavage in patients with primary biliary cirrhosis facilitates subsequent binding of C3 to C3b receptors and targets of complement attack.

Calcium↗
PubMed1989

[Distribution of C3b receptors on polymorphonuclear leukocytes from normal healthy adults by scanning immunoelectron microscopy].

The distribution of C3b receptors on polymorphonuclear leukocytes cultured from normal healthy volunteers was examined by scanning immunoelectron microscopy with mouse anti-CR1 monoclonal antibody and 40 nm-goat anti-mouse IgG antibody. The distribution was categorized into three types; first, Au-particles clustered in numbers of several to ten or more on polymorphonuclear leukocytes (mean +/- S.D. = 59.5 +/- 36.8, n = 146), second, tens of the particles mostly on two or three ruffles of the cells (121.7 +/- 63.8, n = 45), and third, particles assembled at one part of the cells (74.1 +/- 47.4, n = 59). The distribution of Au-particles on all polymorphonuclear leukocytes showed a normal distribution curve (74.1 +/- 50.6, n = 250, p less than 0.02). These results show that polymorphonuclear leukocytes had some tendencies but no uniformity of distribution of C3b receptors on their plasma membrane when they were cultured.

Cells, Cultured↗
PubMed1989

Erythrocyte complement receptor type I in patients with hematologic diseases.

Erythrocyte complement receptor type 1 (CR1) was measured in 37 normal controls and in 95 patients with various hematologic diseases. Levels of erythrocyte CR1 were significantly decreased in patients with acute myelocytic leukemia (AML), acute lymphocytic leukemia (ALL), chronic myelocytic leukemia, non-Hodgkin's lymphoma (NHL), aplastic anemia, idiopathic thrombocytopenic purpura, and multiple myeloma when compared to normal controls. There was also a trend of recovery of erythrocyte CR1 levels in AML and ALL patients when they were in a state of complete remission compared to those at time of onset or relapse. Further investigation is needed as to determine whether the level of erythrocyte CR1 can serve as a predictor for relapse of leukemia. This study also showed that the level of erythrocyte CR1 was not related to prognostic factors in NHL patients.

Erythrocytes↗
PubMed1989

[Preliminary study on the immune function of red cells in patients with pregnancy-induced hypertension].

This study compared the immune adherent function of red cells, circulating immune complex (CIC) and T lymphocyte immune function in cases of pregnancy induced hypertension (30 cases) and normal pregnancy (30 cases). In the former group the rosette rate of red cells C3b receptor was 8.8 +/- 3.2% (normal rate: 19.4 +/- 6.0%), and rosette rate of E-RFC was 46 +/- 2 +/- 7.3% (normal rate: 62.3 +/- 6.4%). In women with normal pregnancy, the former was 16.9 +/- 4.8%, and the latter was 58.0 +/- 8.3%. In women with pregnancy induced hypertension, the immune adherent function of red cells and T lymphocyte immune function were both lower than those in normal pregnant women, while CIC was higher. In normal pregnant women, the immune adherent function of red cells and T lymphocyte immune function were lower than those in the non-pregnant, while CIC was higher. The mechanism and significance of the red cells immunological adherent function in pregnancy induced hypertension were discussed.

Antigen-Antibody Complex↗
PubMed1989

[Flow cytometric measurement of C3b receptors (CR1) on human erythrocytes. II. E-CR1 levels in patients with various diseases and their correlation with B-CR1].

Using a novel technique previously described for measuring erythrocyte C3b receptors (E-CR1) by means of flow cytometry, we studied E-CR1 levels in patients with various diseases. We also measured C3b receptors of B cells (B-CR1) by flow cytometry, and studied the correlation between E-CR1 levels and B-CR1 levels. We have found; 1) Decreased E-CR1 levels were seen in patients with active SLE, acute leukemia, and congenital immunodeficiency syndrome. E-CR1 levels in patients with IgA nephropathy, membranoproliferative glomerulonephritis, anaphylactoid purpura, infectious mononucleosis, and viral pneumonia were statistically higher than those in normal controls. 2) Decreased E-CR1 levels in some patients with SLE were not thought to be inherited, but the E-CR1 levels of patients with diseases other than SLE appeared to be regulated in an autosomal co-dominant form of inheritance. 3) A negative correlation was observed between E-CR1 levels and B-CR1 levels in both patients with SLE and normal controls.

Adolescent↗
PubMed1989

[Preliminary study on red cell immune adherence inhibitory activities in serums of myasthenia gravis patients].

The serum inhibitory activities on RBC-C3b receptor rosette of healthy individuals were studied in myasthenia gravis (MG) patients. The serum inhibitory activities appeared in 65% of MG patients. The serum inhibitory activities of generalized type MG were higher than those of ocular type MG. It was also found that the serum inhibitory activities were correlated with the RBC-C3b receptor rosette rate and immune complex (CIC). Furthermore, it was identified that the CIC of MG serums possessed the inhibitory activity on RBC-C3b receptor rosette.

Antigen-Antibody Complex↗
PubMed1989

[Activity of the red-cell C3b receptor and the circulating immuno-complex in patients of herpes simplex keratitis].

The activity of red-cell C3b receptor and the level of circulating immuno-complex in 35 cases of herpes simplex stromal keratitis were determined, with the results that during the stage of acute attack, the former was significantly lowered, while the level of the latter became markedly higher than that of the controls, and after treatment, the indicators returned to normal values. There was a negative correlation between the red-cell C3b receptor activity and the circulating immuno-complex in serum, indicating that the immuno-function of red-cells in patients with herpes simplex stromal keratitis was impaired and the depression of red-cell C3b receptor activity was one of the reasons for the elevated concentration of circulating immuno-complex in serum.

Adolescent↗
PubMed1989

Regulation of superoxide responses of human neutrophils by adenine compounds. Independence of requirement for cytoplasmic granules.

Recent evidence suggests that the adenine compounds ATP, adenosine-5'-O-(3-thiotriphosphate) (ATP gamma S), and adenosine have important regulatory effects on O2- responses of human neutrophils stimulated with the chemotactic peptide N-formyl-Met-Leu-Phe (fMLP). Because of evidence that receptors on neutrophils may be modified by granule fusion events, we assessed the extent to which these adenine compounds affect fMLP and CR3 (C3bi) receptors on neutrophils and whether cytoplasmic granules are required for the ability of the adenine compounds to modify O2- responses in neutrophils stimulated with fMLP. Incubation of neutrophils with ATP gamma S or adenosine led to a decrease in numbers of fMLP receptors (17 and 9.2%, respectively) but no change in receptor affinity (Kd). Paradoxically, ATP gamma S caused an increase in CR3 receptors (Mo1, CD-11b antigen), suggesting that fMLP and CR3 receptors may be under separate control. The ability of the adenine compounds to modify O2- responses in fMLP-stimulated cells was equivalent in both neutrophils and cytoplasts, suggesting that the regulatory effect of ATP, ATP gamma S, and adenosine do not require the presence of cytoplasmic granules. ATP gamma S caused enhancement of O2- responses of neutrophils to phorbol 12-myristate 13-acetate, raising the possibility that ATP gamma S may be affecting late events in the signal transduction pathway.

Adenosine↗
PubMed1989

Requirement of leukocytic cell adhesion molecules (CD11a-c/CD18) in the enhanced NK lysis of iC3b-opsonized targets.

Treatment of Raji or Daudi cells with human serum under conditions which allow the alternative pathway of C activation results in their C3-opsonization and enhanced sensitivity to NK-mediated lysis. The effector lymphocytes have low buoyant density, carry CD16 and HNK1 markers as well as the CD11a-c/CD18 leukocytic cell adhesion molecules. One of these molecules, made up of CD11b-CD18 (alpha- and beta-chains), is also the receptor for iC3b. We studied the role of the cell adhesion molecules in the NK effect on targets with and without C3-fragments. We focused on the E/T interaction of opsonized cells in the presence of anti CD18 mAb. mAb directed to the CD11a molecule caused 0 to 30% inhibition of the lysis of both non-opsonized and opsonized cells whereas the mAb antibody directed to the CD11c molecule had no effect. Reagents reactive with the iC3b binding site of CD11b (alpha-chain of the CR3) molecule did not alter the lysis of non-opsonized targets whereas they abrogated the C3-mediated increment of the Nk effect on opsonized cells. Two mAb preparations, 60.3 and IB4, directed to the CD18 chain shared by the three cell adhesion molecules abrogated in a dose-dependent way the lysis of both non-opsonized and opsonized targets. The 60.3 mAb inhibited the iC3b binding site of CR3 (despite its localization on the alpha-chain) and in accordance it inhibited the binding of lymphocytes to the opsonized target also. The IB4 did not affect this site and in accordance it inhibited only partially the binding of effectors to the C3 fragment carrying Raji, nevertheless it inhibited their lysis. This result indicates that the iC3b-CR3 bridge is insufficient for triggering the lysis in absence of the contact through the adhesion molecules.

Antibodies, Monoclonal↗
PubMed1989

CR1 polymorphism in hydralazine-induced systemic lupus erythematosus: DNA restriction fragment length polymorphism.

The contribution of genetic factors in the reduction in erythrocyte CR1 levels observed in hydralazine (Hz) induced systemic lupus erythematosus (SLE) was investigated by determining the frequency of a HindIII restriction fragment length polymorphism (RFLP) in the CR1 gene. This RFLP is associated with quantitative erythrocyte CR1 expression. Individuals who have developed SLE as a reaction to Hz therapy, consanguinous relatives of the Hz-SLE patients, controls who had been treated with Hz without any adverse reaction, and the consanguinous relatives of these controls were included in this study. No difference was found in the frequency of occurrence of the alleles associated with CR1 expression between the Hz-SLE patients and the control groups (P greater than 0.2). Individuals from the Hz-SLE group who were homozygous for the 7.4 kb 'high expressor' allele had lower mean levels of erythrocytes CR1 (564 +/- 65) than the corresponding homozygous subgroups within the Hz-SLE relative group (774 +/- 46), the Hz control group (756 +/- 80) and the Hz control relatives group (825 +/- 66). In addition, 50% of the Hz-SLE patients in the 'high expressor' subgroup who had less than 500 CR1 per erythrocyte had elevated levels of circulating immune complexes. This study suggests that individuals who are genetically low expressors of erythrocyte CR1 are not predisposed to developing SLE in response to Hz therapy, and that in a subgroup of genetically 'high expressors', low CR1 levels are associated with elevated levels of circulatory immune complexes.

Alleles↗
PubMed1985

Normal function of CR1 on affected erythrocytes of patients with paroxysmal nocturnal hemoglobinuria.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic anemia in which affected erythrocytes (E) are abnormally sensitive to lysis by autologous complement. Affected E from patients with PNH (PNH-E) are deficient in an E membrane regulatory protein of complement, decay-accelerating factor (DAF). Because a functional defect in a second membrane regulatory protein of complement, CR1 (C3b receptor), has also been hypothesized, severely affected PNH-E (type III PNH-E) were tested for abnormalities in CR1 by four methods. E from two patients with 100% type III PNH-E had 3201 and 6783 sites per cell for binding of 125I-labeled rabbit polyclonal F(ab')2 anti-CR1. These values fall within the normal range of CR1 antigenic sites per cell (1267 to 7915, mean = 5,014 +/- 155 SEM) established by assaying the E from 113 healthy donors. The Ka of CR1 on type III PNH-E for 125I-labeled C3b dimer was 2.06 X 10(7) M-1, and the Ka values for the binding of the same ligand to the E from two healthy individuals were 2.45 X 10(7) M-1 and 1.58 X 10(7) M-1. In an assay designed to measure the capacity of human E (Eh) to accelerate the decay of the classical C3 convertase deposited on 1 X 10(7) bystander sheep E (EAC1gp,4bh,2agp), the half-life (t 1/2) of this convertase was diminished from 18.1 min (range 15.2 to 22.9) to 8.1 min (range 7.4 to 8.5) by the addition of 1 X 10(7) normal Eh, to 6.2 min by 100% type III PNH-E, and to 7.5 min by Eh pretreated with an IgG fraction of human antiserum directed against the D antigen of the Rh system. In contrast, Eh (t 1/2 = 7.4) pretreated with a saturating dose of F(ab')2 anti-CR1, and CR1-deficient Eh (less than 10 CR1 molecules/E) from a patient with systemic lupus erythematosus, showed a loss of convertase decay-accelerating capacity to t 1/2 = 11.6 and t 1/2 = 12.4, respectively. Type III PNH-E pretreated with anti-CR1 demonstrated a total loss of their decay-accelerating capacity (t 1/2 = 19.9). In an assay of I cofactor activity, soluble C3b was rapidly converted to iC3b by purified I plus Eh or type III PNH-E, whereas CR1-deficient Eh exhibited less than 5% the I cofactor activity of normal Eh.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigen-Antibody Complex↗