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At least 703 records · Page 39Linked to original sources
PubMed1998

Effect of macrophage depletion by liposomes containing dichloromethylene-diphosphonate on endotoxin-induced uveitis.

Footpad injection of lipopolysaccharide (LPS) from Salmonella typhimurium in Lewis rats induces an acute anterior and posterior endotoxin-induced uveitis (EIU). To investigate the role of macrophages in the pathogenesis of EIU, we eliminated macrophages by means of liposomes containing dichloromethylene-diphosphonate (Cl2MDP), a drug which depletes macrophages but not other immunocompetent cells. Intravenous injection of CL2MDP-liposomes clearly inhibited clinical and histological manifestations of uveitis in the anterior segment of the eye (iris/ciliary body) and reduced TNF level in aqueous humor. Specific immunostaining showed that CL2MDP-liposome injections decreased the number of ED2 + resident macrophages in the iris/ciliary body and the choroid. After LPS injection, CL2MDP-liposome treatment reduced the density of infiltrating ED1 + cells (mainly monocytes/macrophages) in the iris/ciliary body but not in the choroid; little or no effect was detected on the OX42 + cellular infiltration (mainly polymorphonuclear leukocytes). The inflammatory cellular infiltration of the retina was not modified by the treatment. These findings suggest that macrophages play a key role in the pathogenesis of ocular inflammation.

Analgesics, Non-Narcotic↗
PubMed1999

Immune evasion of tumor cells using membrane-bound complement regulatory proteins.

Membrane-bound complement regulatory proteins (mCRPs) play an important role in the protection of cells from complement-mediated injury. It is now apparent that malignant tumor cells also express these proteins to escape complement attack. Here, Arko Gorter and Seppo Meri discuss the implications of complement resistance for the immunotherapeutic treatment of solid tumors with monoclonal antibodies.

Animals↗
PubMed1994

Lowered expression of C3b receptor (CR1) on erythrocytes of rheumatoid arthritis patients.

The number of C3b receptors (CR1) on erythrocytes (E) has been quantitated by whole cell enzyme-linked immunosorbent assay (ELISA), using a monoclonal anti-CR1 antibody, in 46 healthy individuals as controls, 58 having rheumatoid arthritis (RA) and 3 hereditary angioedema patients. The mean value of CR1 in RA (381/E) was significantly lower (p < 0.001) when compared to normal controls (646/E). In hereditary angioedema patients CR1 numbers (620/E) were found to be comparable to normal values. No significant difference was found between normal male (708/E) and female (598/E) subjects. Among the patient groups, those on steroid therapy (352/E) showed no change compared to others not receiving such therapy (408/E). The cumulative frequency curve of CR1 in the normal population showed maximum inflection at 32% and 82%. This led us to conclude that there is a trimodal distribution of receptors in the control population. Such a contention is well supported by frequency histogram, when a small group interval (0-50) was chosen. However, if large group intervals (0-100 or 0-150) were considered, a very close approximation to unimodal pattern was obtained. The factors actually contributing to low receptor numbers are yet to be elucidated.

Adolescent↗
PubMed1983

Importance of factors H and I for the adherence of C3b-coated erythrocytes to cells.

The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) cells was investigated. Pretreatment of CR+ cells with antibodies to factor H inhibited the adherence of C3b-coated red cells to human tonsil lymphocytes (TL) and peripheral blood monocytes (M phi). The C3b receptor reactivity of human polymorphonuclear leucocytes (PMN) was not influenced and the one of Raji lymphoblastoid cells only slightly influenced; iC3b and C3d receptor reactivity was in no case affected. When diisopropylfluorophosphate (DFP) in a concentration of 0.1 mM was present during pretreatment of the CR+ cells with anti H, the antibodies gained the capacity to inhibit the adherence of C3b-coated erythrocytes to Raji cells; this effect was dose-dependent with respect to DFP. In contrast, there was no influence of DFP on the inhibition pattern of anti H in the case of TL and M phi. The adherence of C3b-coated erythrocytes to PMN remained unaffected by anti-H antibodies in the presence of DFP. Polyclonal as well as monoclonal antibodies directed against human factor I inhibited the binding of C3b cells to Raji cells but not to TL. Additionally, when anti I and anti H antibodies were both present, C3b receptor reactivity of Raji cells was inhibited to a larger extent than with either antibody alone; again, TL remained unaffected. Results obtained by washing the Raji cells before and after treatment with anti H and anti I suggest that the respective antibodies act on factor H primarily on the level of the cell membrane and on factor I in the fluid phase.

Animals↗
PubMed1984

Ehrlich ascites cells activate the alternative pathway of the human complement system.

Incubation of Ehrlich ascites cells with normal or C1q or C2 deficient human sera results in killing of the cells. Killing occurred also in the absence of free Ca++, which supported by the fact that factor B and C3 were cleaved, leads to the conclusion that the alternative pathway of the complement system is activated on the surface of the Ehrlich ascites cells.

Animals↗
PubMed1987

Characterization of the human erythrocyte complement receptor CR1 (C3b receptor) by epitope mapping.

Monoclonal antibodies and an anti-idiotypic serum against human complement receptor CR1 (C3b receptor, immune adherence receptor) were used to identify CR1 and some of its proteolytic fragments by an immunoblotting technique. The anti-idiotypic serum had a specificity for the C3b-binding site, as could be shown by its cross-reactivity with complement factor H. The monoclonal antibodies GARP-4 and GARP-37 were specific for epitopes located nearby the ligand-binding site, because they blocked the immune adherence reaction. For the immunoblotting technique, it was essential to use non-reducing conditions, since reduction of CR1 destroyed the epitopes. Therefore, mainly large (disulphide-linked) fragments of CR1 were obtained. A chymotryptic fragment of Mr 56,000 identified by GARP-4, was the smallest cleavage product to be associated with the C3b-binding domain. Different proteases gave CR1 degradation products of similar Mr, indicating the presence of distinct domains, three of which had a Mr approximately 38,000. A schematic model of CR1 substructure was deduced from the epitope mapping data.

Antibodies, Monoclonal↗
PubMed1985

Mixed-pattern immune deposit glomerulonephritis in a child with inherited deficiency of the third component of complement.

The renal histopathology of a 7-year-old Laotian male with inherited deficiency of the third component of complement, recurrent infections, and persistent hematuria and proteinuria is described. The histologic changes are predominantly those of mesangiopathic disease with isolated changes resembling type I membranoproliferative glomerulonephritis and transmembranous glomerulonephritis. IgG, IgA, IgM, C4, and fibrinogen, but not C3, were detected by immunofluorescence in mesangial zones and in segments of capillary walls. A normal distribution of C3b receptors was present along all capillary walls. This report provides additional support for the association of congenital C3 deficiency and immune deposit glomerulonephritis.

Child↗
PubMed1996

Intercellular adhesion molecule-1/leukocyte function associated antigen-1-mediated and complement receptor type 4-mediated infiltration and activation of glomerular immune cells in immunoglobulin A nephropathy.

Glomerular expression of intercellular adhesion molecule-1 (ICAM1) (CD54) and membrane cofactor protein (MCP; CD46) and positive infiltrating cells in leukocyte function associated antigen-1 (LFA1)alpha (CD11a) and C3bi receptors (CR3/CD11b, CR4/CD11c) were examined by the indirect immunoperoxidase method on 43 sets of repeated renal biopsy specimens from patients with immunoglobulin A nephropathy. Twenty-four-hour urine protein at the time of renal biopsy was also evaluated. Glomerular infiltration of LFA1alpha+ cells was significantly correlated with glomerular expression of ICAM1 (r = 0.494, P < 0.0001). Glomerular complement receptor type 4 (CR4)+ cells were significantly correlated with glomerular expression of MCP (r = 0.405, P < 0.0001). The glomerular expressions of ICAM1 and MCP were significantly correlated with each other (r = 0.700, P < 0.00001). The glomerular infiltrations of LFA1alpha+ and CR4+ cells were highly correlated with each other (r = 0.884, P < 0.00001), and both cell types were significantly correlated with urine protein (respectively, r = 0.426 and 0.478, P < 0.001 and 0.0001). When the change in these parameters between the time of the initial and follow-up biopsies was evaluated, there was a significant correlation between the change in glomerular expression of ICAM1 (DeltaICAM1) and MCP (DeltaMCP) as well as between the change in glomerular infiltration of LFA1alpha+ cells (DeltaLFA1alpha+) and CR4+ cells (DeltaCR4+). Both DeltaLFA1alpha+ and DeltaCR4+ were significantly correlated with the change in urine protein. These findings suggest that ICAM1/LFA1 interaction and MCP-mediated C3bi/C3biR interaction cooperate and participate in persistent glomerular infiltration of immune cells in immunoglobulin A nephropathy, and that these LFA1alpha+ and C3biR+ cells contribute to the induction of proteinuria.

Adult↗
PubMed2000

High-fat diets suppress CD3 and CD25 expression on the surface of murine lymphocytes.

To determine the effects of dietary fats on surface antigen expression, we tested the effects of amount and type of dietary fat on murine lymphocytes. Mice were fed diets with 12 en%, 23 en%, or 47 en% fat containing coconut, olive, safflower, or linseed oil. After 2 wk of ad libitum feeding, the mice were killed and splenic lymphocytes were harvested. Lymphocytes were incubated with fluorescent-tagged monoclonal antibodies and assayed for mean and total surface expression using flow cytometry. Our results show that high-fat (47 en%) diets suppress expression of CD3 and CD25 antigens. We also found that linseed-oil diets suppress expression of CD11a but enhance expression of CD25 antigens. Both CD3 and CD25 are critical for lymphocyte activation, and we conclude that immunosuppression associated with high-fat diets may be associated with suppression of these surface antigens.

Animals↗
PubMed2002

CD35 expression on peripheral blood granulocytes of patients with atopic dermatitis.

We examined CD35 expression on granulocytes from 45 patients with atopic dermatitis (AD) (male, 21, female, 24) and 25 age and sex-matched controls (male, 15; female, 10). There was no significant difference in the peripheral blood neutrophil count between AD patients and controls, whereas the eosinophil count in AD patients was significantly higher than that of controls. The percentages of CD35 positive eosinophils and neutrophils were determined by using two-color flow cytometric analysis. As regards eosinophils, we found CD35 expression from AD patients to be lower than that of controls (P < 0.05), but there was no correlation between the CD35 expression and disease severity. In contrast, the CD35 expression on neutrophils from AD patients was much lower than that of controls (P < 0.005). Furthermore, CD35 expression on neutrophils of severe AD group was significantly higher than that of the mild AD group (P < 0.05). This suggests that the CD35 expression of neutrophils but not eosinophils reflects disease severity in AD patients and the CD35 expression on neutrophils in AD patients may associate with susceptibility to bacterial infection.

Administration, Oral↗
PubMed2003

HUVEC take up opsonized zymosan particles and secrete cytokines IL-6 and IL-8 in vitro.

Uptake of zymosan A particles by human umbilical vein endothelial cells (HUVEC) and its effect on cellular cytokine and oxygen radical production was examined. HUVEC took up more serum-opsonized than -unopsonized zymosan as demonstrated by flow cytometry with fluorescence-labeled particles. The former uptake was inhibited in the presence of anti-C3c antibodies and thus complement-mediated. It probably occurred via CR1 (CD35), although participation of other receptors cannot be ruled out. Scanning electron microscopy indicated that HUVEC with fully internalized zymosan particles were damaged. Prolonged incubation of both serum-opsonized and -unopsonized zymosan particles with HUVEC induced increased secretion of the proinflammatory cytokines IL-6 and IL-8 to the cell culture supernatants, but had no effect on production of oxygen radicals. The results confirm previous reports that EC can internalize yeast and other pathogens and points to complement as a mechanism of uptake, but illustrates that the cells may be damaged in the process. Moreover, EC may participate in the anti-infection defense effort by secreting proinflammatory and chemotactic cytokines in response to the contact with pathogens.

CD11b Antigen↗
PubMed1997

Adherence of Salmonella typhimurium to murine peritoneal macrophages is mediated by lipopolysaccharide and complement receptors.

Adherence of Salmonella typhimurium to mouse peritoneal macrophages (Mø) was monitored using a direct microscopic assay and flow cytometry. Competitive binding studies using wild-type lipopolysaccharide and derivatives confirmed a role for this moiety in bacterial adherence. Mø pretreated with 2-deoxy-D-glucose exhibited lower binding activity than did untreated controls, suggesting involvement of either Fc or complement receptors. Pre-exposing Mø to Fc fragments, however, failed to reduce bacterial binding, thus eliminating a role for Fc receptors in this process. Mø pretreated with neutrophil elastase exhibited a diminished ability to bind S. typhimurium, suggesting involvement of complement receptor 1. Monoclonal antibodies M1/70 and M18/2, specific for epitopes on the alpha and beta chains, respectively, of complement receptor 3, also blocked this adherence. In each case we were unable to eliminate completely bacterial adhesion to Mø. Monoclonal antibodies to two additional Mø receptors, Mac-2 and Mac-3, did not block bacterial attachment. These data indicate that multiple mechanisms are involved in the initial adhesion of S. typhimurium to mouse Mø.

Animals↗
PubMed2000

Immunology of reproduction: protecting the placenta.

The propensity of complement to damage self is controlled by expression of regulatory proteins. Recent results demonstrate that deleting just one of these regulators in mice causes complement to attack and destroy the embryo. These findings may have relevance to human pregnancy.

Animals↗
PubMed1998

Prevention of hyperacute rejection by phosphatidylinositol-anchored mini-complement receptor type 1.

Complement receptor type 1 (CR1, CD35) contains both factor I cofactor activity and convertase decay accelerating activity, but is, in general, thought to be an extrinsic regulator of complement activation. In this study, we prepared a phosphatidylinositol (PI)-anchored mini-CR1, which is composed of the short consensus repeat (SCR) 8-11 of CR1 and the PI anchor of DAF, and expressed it stably on a swine endothelial cell (SEC) line. We then examined the intrinsic regulatory activity of the mini-CR1, with respect to complement-mediated cell lysis as an in vitro hyperacute rejection model of a swine to human discordant xenograft. Flowcytometric profiles of the stable SEC lines with mini-CR1 showed a moderate level of expression for this molecule. Mini-CR1 blocked human complement-mediated cell lysis by approximately 50-70% on SEC. From the data of this study and our previous studies, mini-CR1 was more effective than membrane cofactor protein (MCP, CD46), and as effective as decay accelerating factor (DAF, CD55) in this system. The results suggest that PI-anchored mini-CR1 represents a useful molecule for clinical xenotransplantation.

Animals↗
PubMed1997

Complement receptor type 1 (CR1, CD35) is a receptor for C1q.

Molecular definition of the cellular receptor for the collagen domain of C1q has been elusive. We now report that C1q binds specifically to human CR1 (CD35), the leukocyte C3b/C4b receptor, and the receptor on erythrocytes for opsonized immune complexes. Biotinylated or radioiodinated C1q (*C1q) bound specifically to transfected K562 cells expressing cell surface CR1 and to immobilized recombinant soluble CR1 (rsCR1). *C1q binding to rsCR1 was completely inhibited by unlabeled C1q and the collagen domain of C1q and was partially inhibited by C3b dimers. Kinetic analysis in physiologic saline of the interaction of unlabeled C1q with immobilized rsCR1 using surface plasmon resonance yielded an apparent equilibrium dissociation constant (K[eq2]) of 3.9 nM. Thus, CR1 is a cellular C1q receptor that recognizes all three complement opsonins, namely, C1q, C3b, and C4b.

Binding Sites↗