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PubMedDate not supplied

Inhibition of complement by gold sodium thiomalate.

The effect of gold sodium thiomalate on C3 and factor B activation by monosodium urate monohydrate (MSUM) and zymosan was studied using a quantitative immunoelectrophoretic assay for complement activation. C3 and factor B conversion by the classical pathway activator MSUM, was inhibited 50% and 100% by 3.2 x 10(-4)M and 10(-3)M gold sodium thiomalate, respectively. C3 and factor B conversion by the alternative pathway activator, zymosan, was much less susceptible to inhibition by gold. Gold at 10(-3)M, inhibited alternative pathway activation by only 30%. A 50% inhibition would have required 10(-2)M gold. There was no significant inhibition of complement activation through either pathway by less than 10(-4)M gold. Sodium thiomalate alone showed no inhibition. Studies using other crystals and immune complexes were confirmatory. Thus, there was no appreciable inhibition of the complement system at concentrations of gold attainable in the serum of patients receiving chrysotherapy. The in vivo significance of these findings is unknown.

Complement C3↗
PubMed1980

Isolation and characterization of rat complement factor B and its interaction with cell-bound human C3.

Factor B was isolated from fresh rat plasma by sequential chromatography on QAE-A50, Biorex-70, gel filtration on Sephadex G-200 superfine and rechromatography on QAE-A50. That Brat was isolated in its native form was indicated by its migration during immunoelectrophoresis and by its capacity to react with cobra venom factor (CoVF) in the presence of human D to form a C3 convertase capable of cleaving purified rat C3 and human C3. The recovery of Brat was between 8 and 15%; the final material was homogeneous according to SDS-PAGE analysis. Reduction of Brat with DTT in the presence of urea and SDS did not produce detectable peptides of lower molecular weight. Both reduced and unreduced Brat had an apparent molecular weight of 100,000. An antiserum against Brat induced in rabbits recognized only one protein in fresh rat plasma as indicated by immunodiffusion and immunoelectrophoretic analysis. Zymosan treatment of rat serum resulted in the cleavage of Brat into two fragments with alpha and gamma mobility. Native Brat has a beta electrophoretic mobility. The plasma concentration of Brat in Wistar rats was 215 +/- 38 microgram/ml (mean +/- SD).

Animals↗
PubMed1982

Receptors for complement on echinoid phagocytes. II. Purified human complement mediates echinoid phagocytosis.

The ingestion of sheep erythrocytes (E) coated with specific IgM antibody (EA) and various purified human complement components (EAC 1, EAC 14, EAC 142, EAC 1423b, EAC 43b) by echinoid phagocytes was examined. E, EA, EAC 1, EAC 14 and EAC 142 were ingested at a similar and very low level, while a strong opsonic effect was found by coating red cells with purified C 3 (EAC 1423b and EAC 43b). When erythrocyte-bound C 3b was converted to the hemolytically inactive C 3bi, the opsonic effect was markedly increased. Conversion of C 3bi to C 3d resulted in a total loss of opsonic activity. A similar response pattern was found when binding of erythrocytes to mouse macrophages was recorded. Since it cannot be ruled out that phagocytes convert C 3b to C 3bi by endogeneous C 3 inactivator, it is concluded that echinoid phagocytes display CR3 (C 3bi) and possibly also CR1 (C 3b) receptors, while CR2 (C 3d) receptors are lacking.

Animals↗
PubMed1981

A kinetic analysis of immune-mediated clearance of erythrocytes.

A mathematical expression has been derived that successfully correlates the kinetic data for the immune-mediated clearance of red blood cells. The expression resulted from the solution of differential equations arising from a clearance mechanism that was, essentially, consistent with that described by Schreiber and Frank. The mathematical expression correlated data for both IgG-and IgM-mediated reactions. Four different rate constants appear in the final kinetic equation; these constants, which measure the rates of the various steps in the clearance process, were evaluated by an iterative curve-matching process. The values of the rate constants were found to be dependent upon type of sensitizing immunoglobulin, number of C1-fixing sites, and several known immune system modifiers. Correlation of the derived rate expression with the experimental data provided a critical test for the Schreiber-Frank mechanism and the values of the rate constants provided additional insights into the immune clearance process.

Animals↗
PubMed1980

Decreased Fc and complement receptors on the phagocytes of asthmatic children.

Surface receptors of polymorphonuclear (PMN) and mononuclear phagocytes for Fc portions of immunoglobulins and complement were studied in 57 asthmatic children and 23 normal controls. Erythrocyte-antibody complexes (EA) were used to detect the Fc receptors and erythrocyte-antibody-complement complexes (EAC) to detect complement receptors. Both the mean percentages of PMN and monocyte with Fc and complement receptors of asthmatic children were significantly lower than those of normals. Moreover, in allergic patients both the numbers of PMN with Fc and complement receptors decreased significantly after incubation with allergen.

Adolescent↗
PubMed1995

Terminal complement pathway activation and low lysis inhibitors in rheumatoid arthritis synovial fluid.

OBJECTIVE: To investigate terminal complement activation and lysis inhibitors in rheumatoid arthritis (RA). METHODS: C5a, vitronectin and clusterin were quantitated by enzyme immunoassays in plasma and synovial fluid (SF) in RA (n = 30) and osteoarthritis (OA) (n = 11). RESULTS: In RA the concentration of C5a was 3-fold increased in plasma (21.9 vs 7.2 micrograms/l) and 5-fold increased in SF (7.8 vs 1.7 micrograms/l) compared to OA. The SF/plasma ratios for C5a, vitronectin and clusterin were 0.35, 0.36 and 0.23, respectively, not significantly different in the 2 diseases. CONCLUSION: SF terminal pathway activation in RA combined with low local levels of lysis inhibitors might allow lytic or sublytic attacks on local cells, resulting in inflammation and cell damage.

Arthritis, Rheumatoid↗
PubMed1995

Characterization of a complement receptor 2 (CR2, CD21) ligand binding site for C3. An initial model of ligand interaction with two linked short consensus repeat modules.

Human CR2 (CD21, EBV receptor) is an approximately 145-kDa receptor and a member of the regulators of complement activation gene family. Regulators of complement activation proteins are characterized by the presence of repeating motifs of 60 to 70 amino acids that are designated short consensus repeats (SCR). CR2 serves as a receptor for four distinct ligands. Three of these ligands (complement C3, gp350/220 of EBV, and CD23) interact with the amino terminal 2 of 16 SCR (SCR 1 and 2). Previous studies have determined that at least four sites are important in allowing CR2 to efficiently bind EBV. Two of these sites are also important for binding mAb OKB7, a reagent that blocks both EBV and iC3b/C3dg binding to CR2. We have identified and characterized important sites of iC3b ligand binding by utilizing human-mouse CR2 chimeras, a rat anti-mouse CR2 mAb designated 4E3 that blocks receptor binding to C3, and human CR2-derived peptides. In addition to demonstrating an important role for the same sequence in SCR 1 that is part of the mAb OKB7 and EBV binding site, we have identified a new region within SCR 2 that interacts with C3. These results, when compared with a model of a dual SCR solution structure derived from human factor H SCR, predict that two distinct largely surface-exposed sites on CR2 interact with iC3b. A relative twist of 130 degrees about the long axis of the second SCR in this model would be necessary for these sites to form a single patch for iC3b binding on CR2.

Amino Acid Sequence↗
PubMed1994

Peripheral nerve injury induces Schwann cells to express two macrophage phenotypes: phagocytosis and the galactose-specific lectin MAC-2.

In N mice, peripheral nerve injury is followed by the normal rapid progression of Wallerian degeneration: Schwann cells proliferate and lose their myelin, which is phagocytized and metabolized by blood-borne macrophages. The role of Schwann cells in myelin phagocytosis is debated. Additionally, the molecular mechanisms underlying myelin phagocytosis by the two cell types are not well understood. To elucidate the role of Schwann cells as phagocytes we studied, electron microscopically, in vivo and in vitro degenerating, frozen, and neuroma nerve segments. The major cell types composing these tissues differed: Schwann and macrophages in in vivo degenerating; Schwann in in vitro degenerating; macrophages in frozen; Schwann, macrophages, and fibroblasts in neuroma nerve segments. Both macrophages and Schwann cells phagocytized myelin. We further studied, by immunocytochemistry and immunoblot analysis, the expression of molecules that are characteristically displayed by inflammatory and mature murine macrophages: MAC-1 (the C3b complement receptor), MAC-2 (a galactose-specific lectin), the Fc receptor, and the F4/80 antigen. All were detected in the macrophage-rich, in vivo degenerating, frozen, and neuroma nerve segments. Surprisingly, MAC-2 was also expressed in the macrophage-scarce, Schwann-rich, in vitro degenerating nerve. Immunocytochemistry and immunoblot analysis of isolated non-neuronal cells revealed that both macrophages and Schwann cells displayed MAC-2 on their surface and in their cytoplasm. Morphometry unveiled that galactose and lactose specifically inhibited myelin phagocytosis, as predicted if MAC-2 was mediating myelin phagocytosis by lectinophagocytosis (lectin-mediated phagocytosis). The role of MAC-2 in mediating myelin phagocytosis was further supported by two observations made in W mice that display very slow progression of Wallerian degeneration. First, the failure to degenerate in vivo was associated with deficient MAC-2 production. Second, degeneration that occurred in vitro was associated with MAC-2 production. Furthermore, a strong positive correlation between levels of MAC-2 expression and the extent of myelin destruction by phagocytosis was observed over a wide range of values.

Animals↗