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PubMed1984

The functional characteristics of cultured rat mesangial cell.

Glomerular mesangial cells were isolated from explants of normal rat whole glomeruli according to the differential growth capacities of the cultured cells. The cultured mesangial cells comprised almost all of the grown cells on day 21 of the primary culture when the subculture could be performed. They contained abundant cytoplasmic microfilaments and actin. The contractile response to vasoactive hormone of both primarily cultured and subcultured mesangial cells was quantified as a decrease in cell surface area. The maximum decrease in surface area in response to 1 nM of angiotensin II was about 30%. This magnitude of contraction is consistent with that observed in cultured rat vascular smooth muscle cells. The mesangial cells did not phagocytose horse-radish peroxidase or sensitized sheep red blood cells, nor did they have binding capacities for Fc or C3b, while the cells derived from explanted glomerulus and probably of blood-born monocyte origin did. We conclude that the most important function of the glomerular mesangial cell is the control of glomerular blood flow and filtration by contraction.

Angiotensin II↗

PubMed1987

Regulation of the alternative pathway of human complement by C1q.

The interaction of C1q with C3b and its effect on C3b activities in the alternative pathway of complement (APC) have been studied. Purified C1q markedly inhibited C3b deposition on and lysis of rabbit erythrocytes by the isolated cytolytic APC. It also blocked formation of the C3 convertase, C3b, Bb as well as binding of Factors B and H to sheep erythrocytes (E) bearing C3b. The direct and specific binding of C1q to C3b was clearly demonstrated using the hemagglutination technique at low ionic strength (0.1 M NaCl). C1q concns of 2 micrograms/ml and higher agglutinated, in a dose-dependent fashion, EC3b but not E, EC3bi or EC3d. Addition of C1r and C1s to C1q and formation of C1 did not affect its capacity to agglutinate EC3b. The C1q-mediated agglutination of EC3b was inhibited by EDTA, MgEGTA, C3b and Factor B but not by native C3 or collagen. Heating C1q (56 degrees C) markedly potentiated its agglutinating activity whereas collagenase-treated C1q lost most of its activity. Taken together, these results suggest that C1q binds through its "heads" and in the presence of calcium ions to a site on C3b that is adjacent to the Factor B and Factor H binding sites. This interaction may down-regulate the activity of the alternative pathway of complement on surfaces which activate both the classical and alternative pathways of complement.

Animals↗

PubMed2005

Factor H and atypical hemolytic uremic syndrome: mutations in the C-terminus cause structural changes and defective recognition functions.

Atypical hemolytic uremic syndrome is a disease that is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Mutations in the complement regulator factor H are associated with the inherited form of the disease, and >60% of the mutations are located within the C terminus of factor H. The C-terminus of factor H, represented by short consensus repeat 19 (SCR19) and SCR20, harbors multiple functions; consequently, this study aimed to examine the functional effects of clinically reported mutations in these SCR. Mutant factor H proteins (W1157R, W1183L, V1197A, R1210C, R1215G, and P1226S) were recombinantly expressed and functionally characterized. All six mutant proteins showed severely reduced heparin, C3b, C3d, and endothelial cell binding. By peptide spot analyses, four linear regions that are involved in heparin, C3b, and C3d binding were localized in SCR19 and SCR20. A three-dimensional homology model of the two domains suggests that these four regions form a common binding site across both domains. In addition, this structural model identifies two types of residues: Type A residues are positioned on the SCR surface and are represented by mutants W1157R, W1183L, R1210C, and R1215G; and type B residues are buried within the SCR structure and affect mutations V1197A and P1226S. Mutations of both types of residue result in the same functional defects, namely the reduced binding of factor H to surface-attached C3b molecules and reduced complement regulatory activity at the cell surfaces. The buried type B mutations seem to affect ligand interaction of factor H more severely than the surface-exposed mutations.

Amino Acid Sequence↗

PubMed1984

Metabolic activation of human neutrophils by fluid-phase and particle-bound ligands.

The ability of particle-bound and fluid-phase ligands (IgG, C3b, and ConA) to induce metabolic activation in cytochalasin B-treated human neutrophils was studied. Different activation mechanisms of the neutrophils are proposed, since the activation of cytochalasin B-treated neutrophils is not dependent on whether or not the ligands are particle-bound but not on the nature of ligand per se.

Complement C3b↗

PubMed1982

C1 inactivator and C3b inactivator in peripheral lymph of normal men.

The concentrations of C1 inactivator and C3b inactivator were measured in the peripheral lymph of leg of normal men and compared with the concentrations in serum. Both inactivators were found in lymph, however, in concentrations lower than in serum (lymph/serum ratio for C1INA 0.236, for C3bINA 0.238). The levels of C1INA proteins in lymph were higher than of C1q and C1s (p less than 0.05), and of C3bINA higher or equal to those of C3 and C3PA. This may indicate, that the relatively high concentrations of both inactivators in the extravascular space, as compared with complement component proteins, can play a role in the control of activation process of complement in the interstitium and also explain to some extent the observed low hemolytic activity of lymph C1 and C3.

Adolescent↗

PubMed1985

[Changes in the chemoluminescence behavior of micro- and macrophages in psoriasis: more than just an epiphenomenon?].

Based on previous in vitro examinations, we compared different stimuli eliciting a "respiratory burst" in phagocytes of patients with psoriasis and controls. - Measurements were performed be chemiluminescence (CL). - The results show similar CL in resting phagocytes. Upon stimulation, psoriatic macrophages display augmented CL with aggregated immunoglobulin (aggIg), zymosan (Z), and opsonized zymosan (C3b), macrophages with aggIg, Z, phorbol myristate acetate, and concanavalin A. - The capability for increased phagocytic CL in psoriasis may be modulated by different cell membrane receptors. Changes in the metabolism of arachidonic acid analogous to those encountered in psoriatic epidermis may be responsible for the augmented CL in psoriasis.

Adolescent↗

PubMed1980

[IgG and complement receptors in neutrophils from cord blood (author's transl)].

Percentage of cord blood polymorphonuclear leukocytes (PMN) bearing receptors for Fc portion of the IgG and for complement byproduct C3b are studied in 18 term newborns. Results are compared with those obtained in 20 healthy controls. Statistical analysis did not disclosed significative differences between both groups. Study was performed on total PMN population and not in a selected subpopulation as was done by previous authors.

Complement System Proteins↗

PubMed1992

Peripheral catabolism of CR1 (the C3b receptor, CD35) on erythrocytes from healthy individuals and patients with systemic lupus erythematosus (SLE).

The present study investigated the rate of catabolism of CR1 (the C3b receptor, CD35) on erythrocytes (E) in vivo, in relationship with the expressed number of CR1/E, the CR1.1 HindIII quantitative CR1 polymorphism, and cell age. The relationship between the number of CR1/E and cell age was analysed by measuring G6PDH activity in E that had been sorted according to high or low expression of CR1 (CD35), by assessing the expression of CR1 (CD35) on E separated according to cell density, and by comparing the number of CR1 (CD35) antigenic sites on reticulocytes and on E. A physiological catabolism of CR1 (CD35) manifested by a reduction in the number of CR1 (CD35) antigenic sites/E with cell ageing was consistently observed in healthy individuals. The number of CR1/E decreased with ageing of E according to a complex pattern that associated an exponential decay and an offset. Calculated half-lives of CR1 (CD35) ranged between 11 and 32 days in healthy individuals. A more rapid loss of CR1 (CD35) with cell ageing occurred on cells from individuals expressing high numbers of CR1/E. In patients with systemic lupus erythematosus (SLE), half-lives of CR1 (CD35) on E were in the same range as those of healthy individuals with a similar quantitative CR1 genotype; the number of CR1 (CD35) on reticulocytes was reduced and linearly related to the number of CR1/E, independently of the patients' quantitative CR1 genotype. Transfusion experiments with E bearing high or low amounts of CR1/E indicated the lack of preferential removal of E bearing high numbers of CR1 (CD35) in patients with SLE. These results indicate that the rate of loss of CR1 (CD35) from E with cell ageing is directly related to the quantitative CR1 phenotype and suggest that enhanced peripheral catabolism is not the sole mechanism of the acquired loss of CR1 (CD35) on E in patients with SLE.

Antigens, CD↗

PubMed1989

[C3b-mediated chemiluminescence of human lymphocytes].

Data are presented concerning peculiarities of human lymphocyte luminol-dependent chemiluminescence stimulated with C3b-opsonized and native zymosan. The response was maximal by the 60th min and 4-17 exceeded the results of the negative control. The C3b-opsonization considerably potentiated the lymphocyte activating zymosan's properties and the rate of reaction/maximal level at the 10th min; the effect of phytohemagglutinin reached max by the end of the 1st min in the same tests. The functional significance of the CR- and lectin-mediated structures of lymphocytes is discussed.

Complement C3b↗

PubMed1984

Effect of concanavalin A on intracellular killing of Staphylococcus aureus by human phagocytes.

This study concerns the influence of concanavalin A (Con A) on phagocytosis and intracellular killing of Staphylococcus aureus by human monocytes and granulocytes. Con A binds to S. aureus, monocytes, and granulocytes, and is not opsonic. Con A stimulates the killing of intracellular serum opsonized S. aureus by monocytes, but not by granulocytes. This stimulation of intracellular killing was inhibited by alpha-methyl-mannoside, indicating that the process occurs via Con A specific membrane binding sites. Unlike (tetravalent) Con A, divalent succinyl-Con A does not stimulate intracellular killing, indicating that the lectin valency is important for this stimulation. Con A bound to Sephadex particles, that can not be ingested by monocytes, does not stimulate intracellular killing of S. aureus either, although it, like free Con A, stimulates H2O2 production. Pre-incubation of monocytes with Con A inhibited Fc gamma and C3b-mediated ingestion of S. aureus as well as stimulation of the killing by serum. Divalent Con A had no effect on these functions. This inhibition by Con A is in all probability due to a steric impedance of Con A with respect to the interaction of IgG and C3b with their membrane receptors. Fluorescence techniques showed that Con A was localized on the membrane and in the cytoplasm of the monocytes, whereas granulocytes had only membrane bound lectin. Taken together, these findings suggest that cell penetration by the lectin is obligatory for the stimulation of intracellular killing.

Blood Bactericidal Activity↗

PubMed1995

[Effect of thyroid immune liquor on erythrocyte immune function in patients with autoimmune thyroiditis].

Thirty cases of autoimmune thyroiditis (AT) were treated with thyroid immune liquor (TIL). The results showed that the activity of erythrocyte C3b receptor and erythrocyte immune adherence enhancing factor were significantly increased, while erythrocyte immune complex and erythrocyte immune adherence inhibiting factor were decreased. The thyroid microsome-antibody and thyroid globulin-antibody were also significantly decreased. This indicates that the TIL has adjustive effect on humoral immunity and cellular immunity in patients with AT.

Adjuvants, Immunologic↗

PubMed1983

Membrane Fc-IgG and C3b receptors on myeloid leukaemia cells: a comparison with cytoplasmic acid naphthyl acetate esterase cytochemistry.

Membrane receptors for IgG and C3b were examined on blast cells from 57 cases of acute myeloid leukaemia. These acute leukaemias were classified as myeloblastic, myelomonocytic or monocytic following morphological, cytochemical, and immunological investigations. The membrane receptors of leukaemic blast cells appear to be directly related to the degree of monocytic differentiation with the lowest receptor activities found in acute myeloblastic leukaemia. A comparison was also made between receptor and cytoplasmic acid naphthyl acetate esterase (ANAE) activities in 29 morphologically and immunologically-defined myelomonocytic and monocytic leukaemias. This study revealed that the receptor-positive "monocytic component" in a significant proportion of cases showed unexpectedly weak or negative ANAE reactions suggesting a more cautious approach to the interpretation of ANAE cytochemistry in acute leukaemias. The normal development of cytoplasmic ANAE and membrane receptors is also discussed and compared with their abnormal patterns of expression associated with leukaemic transformation.

Carboxylic Ester Hydrolases↗

PubMed1993

[Eosinophil granule proteins (MBP, ECP, EPX/EDN, EPO)--a possible process of eosinophil activation and degranulation].

From current information, a brief review was made on the basic properties of a possible process of eosinophil activation and degranulation. The "activated" eosinophils show the following characteristics: diminished cell density, morphologic alterations, increased surface receptors, heightened parasite killing, increased metabolic activity and prolonged survival. Immune complexes (secretory IgA, IgG, IgE) are known as potent triggering stimuli of eosinophil degranulation as well as complement fragments (C3b, C3bi). Cytokines (IL-5, GM-CSF), PAF and peptides (substance P) act both as weak degranulation inducer and degranulation enhancer. Synergism between the two pathways, Ca2+ and protein kinase C, is now recognized as a common feature of control of secretion in eosinophils.

Animals↗

PubMed1996

Interleukin-10 inhibits neutrophil phagocytic and bactericidal activity.

Effective host defense against bacterial invasion is characterized by the vigorous recruitment and activation of inflammatory cells, which is dependent upon the coordinated expression of both pro- and anti-inflammatory cytokines. Interleukin-10 (IL-10) is a recently described cytokine with potent anti-inflammatory properties in vivo and in vitro. In this study we investigated whether IL-10 could directly regulate the ability of neutrophils (PMN) to phagocytose and kill bacteria. Initial studies demonstrated that human recombinant IL-10 (hrIL-10) inhibited the ability of PMN to phagocytose Escherichia coli in vitro. Inhibition of phagocytosis occurred in the absence of changes in CR1 (C3b) or Fc receptor expression, as treatment of PMN with IL-10 failed to induce significant changes in Fc gamma IIR, Fc gamma IIIR or CR1 cell surface expression. However, incubation of PMN with IL-10 resulted in a dose-dependent decrease in CDIIb (Mac-1) expression. In addition to effects on PMN phagocytosis, hrIL-10 significantly attenuated PMN microbicidal activity, as bactericidal assays revealed that co-incubation of PMN with hrIL-10 resulted in a marked decrease in killing of phagocytosed bacteria. Furthermore, IL-10 inhibited the production of superoxide from PMA-stimulated PMN, suggesting that the detrimental effects of IL-10 on PMN microbicidal activity were due, in part, to suppression of respiratory burst. In summary, our studies indicate that IL-10 inhibits PMN-dependent phagocytosis and killing of E. coli in vitro, and suggest that this cytokine may impair effective antibacterial host defense in vivo.

Complement C3b↗

PubMed1986

Opsonic receptor function is reduced on the surface of newborn alveolar macrophages.

Neonates have an increased susceptibility to infections. Because optimal phagocytosis of offending organisms by alveolar macrophages (AM) requires recognition and attachment of opsonized organisms to the AM cell membrane, the expression of opsonic receptors on the surface of newborn and adult rat AM was investigated using immunologic techniques, cell culture, and flow cytometry. We investigated the expression of Fc, C3b, fibronectin, and lectin receptors on newborn (1 to 5 wk) AM and compared them with those of adult AM. The expression of Fc receptors (FcR) was significantly less on the surface of newborn AM, particularly during the first week of life, as determined by their binding of aggregated IgG, E(IgG), and opsonized 125I-Listeria monocytogenes. A similar depressed receptor function was observed for C3b, fibronectin, and some lectins. The possible effect of cell size on receptor expression was examined by morphometry and flow cytometry. The results indicated that, while mean AM size was approximately 12% smaller during the first week of life, it attained adult levels by the second week. Thus, a difference in size did not account for either the magnitude of decreased receptor expression or the diminished intensity of staining for surface-aggregated IgG that was detectable for up to 5 wk. Binding of a variety of lectins to the AM surface was decreased during the first week after birth, but approximated adult levels by 4 wk. By contrast, soybean and peanut agglutinin, lectins that bind to D-GaINAC moieties, showed a transient increase in binding to AM during the second and third weeks of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

Interaction of C3 and C3b with immunoglobulin G.

Human C3b as well as native C3 were found to bind to solid phase human and rabbit IgG. Haemolytically active C3 had significantly higher binding capacity to IgG than the C3b fragment. Inhibition experiments proved that C3 and C3b have common binding sites on the Fab and Fc part of the IgG molecule but the character of these binding sites was different. As a functional consequence of C3-IgG interaction, C3 binding was found to inhibit the specific precipitation of an IgG antibody preparation.

Animals↗

PubMed1991

Internalization pathway of C3b receptors in human neutrophils and its transmodulation by chemoattractant receptors stimulation.

On the surface of phagocytes, C3b receptors (CR1) bind C3b-coated particles and promote their ingestion after activation by appropriate stimuli such as lymphokines or the chemoattractant formyl methionyl leucyl phenylalanine (fMLP) and fibronectin. The aims of the present study were 1) to define at the electron microscopic level the nature of the process responsible for CR1 internalization and 2) to dissect the mechanism by which a physiological activator (fMLP) stimulates this process. CR1 was visualized either by the immunogold technique or by quantitative electron microscopic autoradiography using a monoclonal anti-CR1 antibody. Both techniques revealed that after anti-CR1 binding, CR1 cluster on the neutrophil surface in a time-, temperature-, and antibody-dependent fashion, but do not concentrate in coated pits. CR1 internalization requires receptor cross-linking (does not occur in the presence of Fab fragments of anti-CR1) and intact microfilaments. It results in the association of the internalized material with large flattened vacuoles, organized in stacks. Together with the surface localization of CR1 close to cytoplasmic projections (ruffles), these observations suggest that uptake of CR1 occurs through a macropinocytotic process. Eventually, CR1 concentrate in lysosomal structures. fMLP markedly stimulates this pattern of CR1 internalization without affecting their clustering or their lack of association with coated pits. Stimulation by fMLP is inhibited by pertussis toxin, unaffected by preventing receptor-triggered cytosolic free calcium [Ca2+]i elevations, and mimicked by phorbol myristate acetate. Taken together our data demonstrate 1) that, in neutrophils, CR1 is internalized via a coated pit independent macropinocytotic process, dependent on intact microfilaments and receptor cross-linking; 2) that, in the same cells, fMLP is internalized via the classical coated pits pathway; and 3) that fMLP amplifies CR1 uptake possibly via protein kinase C stimulation.

Autoradiography↗

PubMed1978

Characterization of mononuclear cell infiltrates in psoriatic lesions.

The dermal mononuclear cell infiltrates of psoriatic lesions were characterized by receptors for sheep erythrocytes (T-lymphocytes), C3b receptors (macrophages and B-lymphocytes) and C3d receptors (B-lymphocytes), using hemadsorption to cryostat sections in a closed chamber. T-lymphocytes and macrophages were the predominant inflammatory cells. Very few B-lymphocytes were detected. These findings are discussed in relation to the possible pathogenetic signficance of cellular immunity in psoriasis.

B-Lymphocytes↗