Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement C3c”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources

Activation of the alternative pathway of complement by cellulosic hemodialysis membranes.

Compared to cellulose acetate, hemodialysis with cuprophan membranes is associated with greater activation of the alternative pathway of complement. Previous studies have shown that this difference is not due to a greater number of potential covalent binding sites for activated C3 on cuprophan. To investigate further the factors that influence complement activation by hemodialysis membranes, proteins were eluted from serum-treated cuprophan and cellulose acetate membranes with hydroxylamine at alkaline pH and analyzed by SDS-PAGE and Western blot. Approximately 23 times more total protein was removed from cellulose acetate. Virtually all the C3 in the cellulose acetate eluate was in the form of inactive fragments C3c and C3dg. In contrast, the functionally active form of C3 (C3b) was a prominent constituent of the cuprophan eluate. The binding of factor B (precursor of the catalytic subunit of the C3 convertase) and factor H (regulatory protein of C3 activation) to serum-treated membranes was also analyzed. By Scatchard's method, the affinity constant at equilibrium for factor B binding (KB) to the two types of membranes was not significantly different; however, there were approximately four times more factor B binding sites on the cuprophan than on the cellulose acetate. For cuprophan, the number of factor B binding sites was 1.6 times greater than the number of factor H binding sites. These studies demonstrate that a portion of the C3b molecules that bind to cuprophan are protected from degradation, and suggest that the complement activating capacity of hemodialysis membranes is determined by biochemical properties that modulate both the binding of serum proteins to the membrane and the interactions of the endogenous regulatory proteins with membrane-associated C3b.

Cellulose↗

Circulating immune complexes, complement activation kinetics and serum sickness following treatment with heterologous anti-snake venom globulin.

Consecutive serum and plasma samples, from a patient receiving 100 ml polyvalent horse anti-venom globulin after a rattlesnake bite, were analysed for circulating immune complexes (IC) and activation of complement factors. IC were determined by two independent methods, a complement consumption assay and a Clq-binding assay. Rapidly rising levels of complement-fixing circulating IC were detected as early as 4--5 days after the serum treatment and distinct IC-activity was recorded in both assays on day 8 when clinical symptoms of serum sickness were observed. The IC remained in circulation for at least 5 weeks. Signs of intravascular C-activation in the form of low C3, C4 and C5 values was noted on day 1 after treatment. Factor B was demonstrable 3--4 days after the snake bite and this factor and C3c attained a peak around day 8, just before maximal suppression of native C3 and C4. 14 days after the globulin treatment C3c and B were declining rapidly while C3 and C4 approached normal values first 36 days after treatment. An increase in heterophilic antibodies to sheep erythrocytes was observed after treatment with anti-venom globulin.

Adult↗

[Selective binding in vitro of a modified form of the C3 component of complement to human erythrocytes].

C3 was bound to human erythrocytes from autologous plasma or from serum brought to low ionic strength (mu less than or equal to 0.03) and pH between 4.0 and 5.0, then subsequently incubated with erythrocytes (50/1, v/v) for 20 min at 0 degree C. This capacity was preserved up to 72 h by prolonged incubation at 20, 25 or 37 degrees C, whereas it was quickly lost by incubation at 0 degree C. C3 binding did not require complement activation and was not observed with neuraminidase-treated erythrocytes. Crossed immunoelectrophoretic analysis of the pretreated serum or plasma revealed that a fraction having more cathodal migration than that of native C3 was generated upon incubation in the above-mentioned conditions. This fraction appeared able to selectively bind to the erythrocytes. Cell-bound C3 reacted positively to antisera against C3a, C3c, C3d or native C3; they rosetted positively with EAC3b, clearly showing that this C3 binding was not dependent on the proteolysis of C3 and that it concerned the acceptor sites on the cells, since C3b receptors were free. The functional significance of this C3 binding was also investigated: EC3 were not able to lyse through the alternative pathway, whereas lysis clearly increased when C3 was found to AET-treated erythrocytes. This finding, together with the modulation in the capacity of EC3 or E(AET)C3 to form an alternative pathway convertase by antibodies to C3c or C3d, strongly suggests a contribution of bound C3 to such a convertase. In contrast to "C3b-like" C3, this modified C3 was able to bind to acceptor sites on erythrocytes but, like the former, it retained the capacity to form an alternative pathway convertase. In this light, it may represent an intermediate between C3 and "C3b-like" C3.

Complement Activation↗

Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE): serial analysis in relation to disease course.

The levels of IgA, IgG and IgM immunoconglutinins (IK) were assessed in sera from 20 patients with SLE which were followed for 8-month periods. At the time of the exacerbation, IgG IKs were significantly increased to 226 +/- 90 arbitrary units (mean +/- s.e.m.) compared with both the minimum value of 75 +/- 28 in the SLE patients and with 31 +/- 2 in healthy controls (P < 0.05). There was no difference between SLE patients and controls in the levels of IgM and IgA IKs. Most of the SLE patients in this material showed maximal IgG IK levels before exacerbation, but there was no correlation between the clinical disease index and the levels of IgG IK. The specificity of IgG IKs showed a broad diversity for microtitre-fixed C3b, iC3b, C3c and C3dg. The antibodies were of IgG1, IgG3 and in two patients, IgG4 subclass. IgG IKs were correlated to the C3d/C3 ratio which suggested that the IK responses were secondary to C3 activation. In summary, unlike other conditions associated with complement activation where elevated IgM IKs are common, an increase in IgG IK levels was observed. It is possible that this diverging IK response contributes to the pathophysiology of the disease.

Antibody Specificity↗

Hypocomplementemic proliferative glomerulonephritis with C3 nephritic-factor-like activity in multiple myeloma.

Advanced renal failure, nephrotic-range proteinuria due to proliferative glomerulonephritis and multiple myeloma with circulating IgG2 lambda and free lambda light-chain paraproteins occurred in a 31-year-old male. Commonly established causes of renal failure in multiple myeloma were excluded. Immunofluorescence revealed heavy granular glomerular deposition of C3. Serum C3 was decreased, and C3c was increased. C3 nephritic-factor (C3 NeF)-like activity was demonstrated in the serum. Plasmapheresis and chemotherapy resulted in a decrease in paraprotein concentration up to 90%, a decrease in C3 NeF-like activity to negligible, normal serum complement levels and a marked improvement in both renal function and proteinuria. With reference to the literature, the possibility of a syndrome of paraproteinemia, C3 NeF-like activity and glomerulonephritis is forwarded.

Adult↗

Demonstration of the complement regulating protein, beta 1H, in skin biopsies from patients with bullous pemphigoid.

beta 1H-globulin is a recently characterized plasma protein which regulates the biologic activities of the major fragment of the third complement component, C3b. The major function of this protein is to act as a co-factor for C3b Inactivator (C3bINA) in the cleavage of C3b to an intermediate molecule, C3b', consisting of an intact beta-chain covalently bound by disulfide bridges to 2 alpha-chain fragments of 40,000 and 67,000 daltons. Final cleavage of C3b' to the C3c and C3d fragments requires an additional protease such as plasmin or elastase. Additionally, beta 1H interferes with the activity of the alternative pathway convertases, C3bBb and C3bBbP, by displacing or competing with the binding of factor B. In this study, perilesional skin biopsies from 10 patients with active bullous pemphigoid were examined for the presence of beta 1H at the dermal-epidermal junction by immunofluorescent methods. The protein was found in 8 of 9 biopsies in which C3 also was deposited. In a single case where C3 was not found, beta 1H was not seen. These findings suggest that beta 1H plays a role in the in vivo control of C3b and provides additional evidence for the participation of the complement system in the pathogenesis of bullous pemphigoid.

Aged↗

A novel cleavage product of human complement component C3 with structural and functional properties of cobra venom factor.

The generation of two cleavage products of human C3, termed C3o and C3p, by incubation with a C3-cleaving protease isolated from cobra venom (Naja naja siamensis) is described. The venom protease removes the C3p fragment (Mr approximately 33,000) from the C3dg region of the C3 alpha-chain. The major cleavage fragment C3o (Mr approximately 140,000) contains the unaltered beta-chain of C3 and two alpha-chain-derived polypeptides of Mr approximately 29,000 and Mr approximately 38,000, respectively. Amino-terminal amino acids sequence analysis of C3p and the three chains of C3o allowed the identification of the exact location of the two alpha-chain-derived fragments of C3o and the three cleavage sites of the venom protease. The chain structure of C3o resembles those of C3c and cobra venom factor. In contrast to C3c but like cobra venom factor (and C3b), C3o was found to support the activation of the serine protease Factor B by cleavage in the presence of Factor D and Mg2+ into Bb and Ba, generating an enzymatically active complex that is able to cleave a fluorogenic peptide substrate for C3 convertases. Since the only stretch of amino acid residues of C3o not present in C3c is the carboxyl terminus of the Mr approximately 29,000 chain of C3o, it is suggested that this region is important for the interaction with Factor B and convertase formation.

Amino Acid Sequence↗

Precipitable immune complexes in Hodgkin's disease.

Sera from 28 untreated patients with Hodgkin's disease and from 120 healthy controls were investigated for the presence of circulating immune complexes using a modified 3% polyethylene glycol precipitation method with subsequent quantification of the precipitated protein. Elevated levels of precipitable protein were found in 79% (p less than 0.005) of Hodgkin's disease sera. The degree of elevation was associated with disease activity including the presence of B-symptoms. Constant and pronounced increase of precipitable protein was found in six patients with stage-III B nodular sclerosis subtype, thus exceeding the average amount of precipitable protein in healthy controls by a factor of 3-4. The erythrocyte sedimentation rate in 20 patients correlated with the amount of precipitable protein (r = 0.79). Additionally, partial component analysis of the precipitates was carried out by laser nephelometry. Immunoglobulins and complement components were identified as being major components of the precipitated material in sera both from patients and healthy controls, thus confirming the probability of the immune complex nature of the precipitates. Significant differences between patients and healthy controls concerned the amount of precipitable components. Elevation of precipitable IgM was found to be the most sensitive parameter (86% above means + 2 SD of normal controls, p less than 0.005). Increased amounts of precipitable IgG, C4, and Clq were found in 57-46% of patients' sera. Elevation of precipitable IgA and C3c were identified less often. The results suggest the quantification of precipitable immune complexes and their components to be of value as adjuncts in determining disease activity in Hodgkin's disease.

Adolescent↗

Characterization of a soluble form of the C3b/C4b receptor (CR1) in human plasma.

A radioimmunoassay with the use of soluble 125I-Fab monoclonal anti-CR1 and rabbit IgG anti-CR1 bound to Staphylococcus aureus particles was employed to detect and quantitate CR1 antigen in human plasma. Among 16 normal individuals the concentration of soluble CR1 in plasma ranged from 13 to 81 ng/ml, and a similar range of concentration was found in plasma from 15 patients having systemic lupus erythematosus (SLE). The amount of plasma CR1 in normal donors, but not in SLE patients, significantly correlated with the number of CR1 sites on erythrocytes (r = 0.90, p less than 0.001), and was 7.1% of the amount of receptor that was present on erythrocytes in blood. The concentration of soluble CR1 was not diminished by ultracentrifugation or ultrafiltration of plasma, was not affected by various modes of anti-coagulation or even by clotting of blood, and did not change during incubation of blood at 4 degrees C for up to 4 hr. On sucrose density gradient ultracentrifugation of plasma the CR1 was distributed as a broad peak that overlapped the plasma protein profile. The Mr of plasma CR1 was identical to that of erythrocyte CR1 when assessed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and immunoblotting. In addition, the plasma form of CR1 exhibited the same structural phenotype as did receptor from erythrocytes of the same individual. CR1 antigen purified from plasma was as active as CR1 from erythrocytes in promoting the cleavage by factor I of C3b to iC3b, C3c, and C3dg. Therefore, a functionally and structurally intact form of soluble CR1 resides in plasma.

Animals↗

Effect of age-dependent enzymatic degradation of zymosan into oligosaccharides during incubation with serum on its opsonization by complement.

Incubation of zymosan particles with serum was shown to be accompanied by their partial breakdown into the oligosaccharides maltose, maltotriose, and maltotetraose, that were quantified under the form of glucose after degradation by alpha-glucosidase. Incubation with normal adult serum yielded twice as much glucose than incubation with cord serum. The degradation of zymosan could be mimicked by incubation with purified pancreatic alpha-amylase. A correlation was also found between the amount of oligosaccharides released from the particles during their incubation with serum and the concentration of amylase in the sera. The latter is low in newborns and increases several-fold, to nearly adult levels, at 3-6 months of age. Preincubation of zymosan with purified pancreatic alpha-amylase resulted in an approximately 50% increase in the binding of radioactive anti-C3c in the supernates obtained after subsequent incubation with cord serum but not with adult serum. With six of 24 cord sera, but not with adult serum, it also resulted in an augmentation of the chemiluminescence accompanying the phagocytosis of the particles after their opsonization. It is concluded that the relative inefficiency of cord and newborn serum in opsonizing zymosan is attributable not only to their lower content of the components of the alternative pathway of complement, but also to a lower concentration of serum amylase.

Adult↗

Calcium-dependent and calcium-independent signals in the conglutinin-binding assay (KgBa) for immune complexes. Influence of anti-collagen-antibodies.

A solid phase ELISA conglutinin-binding assay (KgBa) was evaluated for the detection of circulating immune complexes. ELISA wells were coated with purified bovine conglutinin and incubated with test sera. Bound IgG was detected with enzyme labelled anti-immunoglobulin. Heat aggregated IgG which had been "solubilized" (i.e., complement treated by incubation with serum) was employed as a reference. The binding of the complement-reacted IgG to solid phase conglutinin was found to be calcium-dependent and inhibitable with N-acetyl-D-glucosamine (GlcNAc). Prolonged incubation (4 days) of aggregated IgG with serum at 37 degrees C abolished the binding to conglutinin, a finding consistent with the complete degradation of deposited C3b to C3c and C3d. The solubilized IgG that bound to solid phase conglutinin was found by gel chromatography to be of high molecular weight (greater than 600 kDa). Binding of IgG to solid phase bovine conglutinin was also observed to a variable degree in normal and pathological sera. However, in this situation the IgG binding was largely calcium-independent, was not inhibited by GlcNAc and did not decrease after prolonged incubation of the serum at 37 degrees C. The reactive IgG eluted on gel chromatography at the position of monomeric IgG suggesting binding via the antigen binding sites. Binding of this IgG was inhibited by both collagen type II and purified conglutinin. These observations suggest that the assay detects cross-reacting autoantibodies against collagen epitopes, or, alternatively, antibodies against the dietary antigen, bovine conglutinin.

Acetylgalactosamine↗

A comparison of fetal and adult porcine islets with regard to Gal alpha (1,3)Gal expression and the role of human immunoglobulins and complement in islet cell cytotoxicity.

BACKGROUND: It is still debated whether fetal or adult porcine islets should be the preferred choice for future clinical islet xenotransplantation. Each type of islet preparation has advantages and disadvantages compared with the other. Here we present a direct comparison between fetal and adult porcine islets with regard to Gal alpha(1,3)Gal expression, immunoglobulin and complement binding, and cytotoxicity after exposure to fresh human serum. METHOD: Islet single cell suspensions were prepared from adult and fetal islets by trypsin digestion. Fluorescein isothiocyanate-conjugated Bandeiraea simplicifolia isolectin B4 (BS-IB4) and affinity-purified chicken anti-Gal alpha(1,3)Gal antibody was used to detect Gal alpha(1,3)Gal expression. Immunoglobulin and complement binding to the islet cells and cytotoxicity for islet cells was compared after incubation with fresh and heat-inactivated human sera and with an immune serum from a diabetic patient who received a fetal porcine islet transplant. Furthermore, two pools of human AB sera were depleted of porcine endothelial cell cytotoxic human anti-Gal alpha(1,3)Gal antibodies by absorption and were used to analyze the effect of Gal alpha(1,3)Gal antibody removal on islet cell cytotoxicity. RESULTS: Fetal islet cells readily bound both BS-IB4 and the chicken anti-Gal alpha(1,3)Gal antibody. None of 10 adult porcine islet preparations were stained by BS-IB4. In comparison, IgY anti-Gal Ab binding was detected in two of eight adult islet isolations, whereas the other six preparations showed marginal/no binding. After incubation of fetal islet cells with fresh human serum, C3c binding was strongly positive and IgM binding variable, with occasional binding of IgG and no detectable binding of IgA. Adult islet cells were also strongly positive for C3c but did not bind detectable amounts of IgM, IgG, or IgA. Immune sera from a patient who had received fetal porcine islets showed the presence of induced antibodies that bound to fetal islet cells and to porcine peripheral blood lymphocytes, whereas binding to adult islet cells was barely detectable. Fresh human sera showed a high and similar level of complement-mediated lytic activity for both adult islet cells (78+/-22%) and fetal islet cells (75+/-16%). Cytotoxicity for fetal islet cells and peripheral blood lymphocytes was significantly reduced when the corresponding sera were depleted of anti-Gal antibodies before use (P=0.002 and P=0.003, respectively). In contrast, no difference in cytotoxicity for adult islet cells was detected when anti-Gal-depleted human sera were used. CONCLUSION: Gal alpha(1,3)Gal expression is occasionally detectable on adult porcine islet cells, but not as readily and at a lower level, compared with fetal islet cells. Thus, as porcine fetal islets mature to adult islets, the expression of the Gal alpha(1,3)Gal epitope gradually diminishes. Consequently, cytotoxic anti-Gal alpha(1,3)Gal antibodies in human serum play an important role in the lysis of fetal but not adult porcine islet cells.

Aging↗

A monoclonal antibody against human complement component C3: the production of C3 by human cells in vitro.

A monoclonal antibody (WM1) against the third component of human complement (C3) was produced by fusing P3-X63-Ag8 mouse myeloma cells with spleen cells from BALB/c mice immunized with purified C3. The specificity of WM1 antibody against C3 was established by its capacity to inhibit a standard C3 hemolytic assay and to immunoprecipitate C3 from human serum in the presence of S. aureus bacteria. Indirect binding assays indicate that the antibody is directed the C3c portion of C3. The immunoprecipitation technique was used to screen for the presence of C3 in the culture supernatants of various cell lines. By this means, C3 was identified as a secreted product of human primary fibroblasts, transformed fibroblasts and D98/AH-2, a HeLa derivative, but not of other human cell lines. WM1 was unable to immunoprecipitate C3 from rabbit or mouse fibroblast culture supernatants.

Animals↗

Construction, expression and functional analysis of a glycolipid-linked form of CR1.

By genetic engineering of human CR1 cDNA and its stable transfection into cells we have produced a cell line which expresses CR1 anchored to the cell surface by a glycolipid anchor. The glycosyl-phosphatidylinositol (GPI)-CR1 protects cells intrinsically from damage mediated by complement activated through the classical pathway. Cell surface GPI-CR1 is more efficient on a molar basis than soluble CR1 in the assay, but extrinsic protection of other cells was not obtained. Soluble CR1-protected cells extrinsically in the assay but was required at nearly ten fold higher amounts than the intrinsic protection conferred by GPI-anchored CR1. Additionally, GPI-CR1 was shown to act as a co-factor to Factor I in the generation of C3c from iC3b. Since GPI-anchored proteins can incorporate spontaneously into the membranes of living cells by virtue of their lipid tails, the isolated GPI-CR1 will be used to introduce CR1 on to the surfaces of many different types of cell so that its role in immunity can be further investigated.

Animals↗

A cleavage product of mouse C3 adsorbable to (1----3)-beta-D-glucan from Alcaligenes faecalis var. myxogenes IFO 13140.

By using affinity chromatography of TAK, a gel-forming antitumor (1----3)-beta-D-glucan produced by Alcaligenes faecalis var. myxogenes IFO 13140 also known as an activator of the alternative complement pathway (ACP), we obtained from mouse serum a cleavage product of C3 (tentatively designated as C3X). Binding between C3X and TAK seemed to be noncovalent. In contrast to C3, C3X had an intact beta chain (70,000 daltons) and instead of an alpha chain, two peptide chains (40,000 and 30,000 daltons) linked by disulfide bonds. C3X retained a portion of C3 antigenicity. By trypsinolysis C3 yielded a fragment similar to C3X on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These results suggest that C3X is C3c. Since C3X was obtained by elution with a high salt solution from TAK incubated with ethylenediaminetetraacetate (EDTA)-serum (serum containing EDTA) but not from TAK incubated with EDTA-plasma, C3X could already be present in the serum before the activation of ACP by TAK.

Adsorption↗

Herpes simplex virus glycoprotein C: molecular mimicry of complement regulatory proteins by a viral protein.

Herpes simplex virus (HSV) encodes a protein, glycoprotein C (gC), which binds to the third complement component, the central mediator of complement activation. In this study the structural and functional relationships of gC from HSV type 1 (HSV-1) and known human complement regulatory proteins factor H, properdin, factor B, complement receptor 1 (CR1) and 2 (CR2) were investigated. The interaction of gC with C3b was studied using purified complement components, synthetic peptides, antisera against different C3 fragments and anti-C3 monoclonal antibodies (mAb) with known inhibitory effects on C3-ligand interactions. All the mAb that inhibited gC/C3b interactions, in a differential manner, also prevented binding of C3 fragments to factors H, B, CR1 or CR2. No blocking was observed with synthetic peptides representing different C3 regions or with factor B and C3d, whereas C3b, C3c and factor H were inhibitory, as well as purified gC. There was no binding of gC to cobra venom factor (CVF), a C3c-like fragment derived from cobra gland. Purified gC bound to iC3, iC3b and C3c, but failed to bind to C3d. Glycoprotein C bound only weakly to iC3 derived from bovine and porcine plasma, thus indicating a preference of the viral protein for the appropriate host. Binding of gC was also observed to proteolytic C3 fragments, especially to the beta-chain, thus suggesting the importance of the C3 region as a binding site. Purified gC from HSV-1, but not HSV-2, inhibited the binding of factor H and properdin but not of CR1 to C3b. The binding of iC3b to CR2, a molecule involved in B-cell activation and binding of the Epstein-Barr virus, was also inhibited by the HSV-1 protein. As factor H and properdin, the binding of which was inhibited by gC, are important regulators of the alternative complement pathway, these data further support a role of gC in the evasion of HSV from a major first-line host defence mechanism, i.e. the complement system. In addition, the inhibition of the C3/CR2 interaction may suggest a possible immunoregulatory role of HSV glycoprotein C.

Antibodies, Monoclonal↗

The cellular component in the parietal infiltrate of inflammatory abdominal aortic aneurysms (IAAA).

Eight cases of inflammatory abdominal aortic aneurysm (IAAA) (group I) and a control group of ten cases of atherosclerotic abdominal aortic aneurysm (AAA) with little or no parietal inflammatory infiltrate (group II) were studied; using light microscopy, transmission electron microscopy (TEM), and immunohistochemistry. These were used to define cell composition in the inflammatory process, the degree of cell activation and alteration of connective tissue. Large numbers of B lymphocytes were present in IAAA with preservation of the T4/T8 ratio. In addition, HLA-DR and the IL2-R antigen (specific for activated cells) were widely expressed in the cell population. The interstitial matrix contained deposits of IgG, IgM and C3c together with an increase in type III collagen and a reduction in elastin which appeared fragmented and swollen. This study, therefore, characterised the cellular component of the parietal inflammatory infiltrate in IAAA. The degree of activation shown by these cell elements and the activation of complement suggest that the relevant antigen may have been localised in the aneurysm wall at the time of observation.

Aged↗

Immune complement activation on polystyrene and silicon dioxide surfaces. Impact of reversible IgG adsorption.

We have studied aspects of the molecular background to immune complement activation on solid surfaces. Quartz crystal microbalance with dissipation monitoring (QCM-D) sensor surfaces were modified by means of spin coating with polystyrene (PS) or sputtering of silicon dioxide (SiO2). The IC activation on modified QCM-D surfaces was investigated by incubation in serum, followed by determinations of the amounts of bound C3 fragments (C3c) at the surface. Determinations of soluble C3a and soluble C5b-9 complex (sC5b-9) were made with enzyme immunoassay (EIA) method. We found that IC activation was high on PS surfaces, independent of the method used for measurements. On the SiO2 surfaces, IC activation was generally lower, but still detectable with anti-C3c as well as sC5b-9 and C3a determinations. Pre-coating the surfaces with a layer of IgG resulted in that IC activation became very high on PS surface, while the IC response remained low on SiO2 surfaces. The lower level of IC activation on the SiO2 surfaces was explained by a low surface concentration of IgG as measured with QCM-D. This was a result of the high reversibility of the IgG protein adsorption as well as absence of sufficient conformational changes of adsorbed IgG molecules. The QCM-D method was as sensitive as the C3a and sC5b-9 determinations to reveal surface associated IC-activation on these model surfaces. Additional advantages of the QCM-D method are the broad dynamic measurement window, i.e. the high precision and the ability to perform time resolved measurements and the ease of making different surface modifications.

Adsorption↗