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 505 records · Page 28Linked to original sources
PubMedDate not supplied

Seminal plasma-induced suppression of the respiratory burst of polymorphonuclear leukocytes and monocytes.

Based on recent findings indicating suppression of lymphocytic functions by seminal plasma (SP) we tested the effects of SP from men with normo- and oligozoospermia (n = 7, each) on the generation of luminol-enhanced chemiluminescence (CL) of polymorphonuclear leukocytes (PMN) and monocytes (M psi) stimulated in vitro with zymosan. We found a complete suppression of CL of PMN and M psi by undiluted SP's, 1,000-fold dilutions still induced greater than or equal to 20 percent inhibition. There was no difference between normo- and oligozoospermic men in inhibition of CL both with PMN and M psi. Protein concentrations of SP's were closely the same; all SP were free of the complement components C4 and C3c. After dialysis of SP the inhibition of PMN - and M psi - generated CL was no longer present. Our results demonstrate that SP exerts extremely potent inhibition of cells mediating nonspecific defense and/or antigen presentation. The inhibitor appears to be of low molecular weight. These findings may be important for infections acquired by the genital tract and may provide an explanation for the immunotolerance of spermatozoa in the female reproductive system.

Complement System Proteins↗
PubMed1994

Bovine conglutinin binds to an oligosaccharide determinant presented by iC3b, but not by C3, C3b or C3c.

Bovine conglutinin is a serum lectin that agglutinates erythrocytes preincubated with antibodies and complement. This agglutination occurs through the binding of conglutinin to iC3b, a fragment of the complement component C3. It was reported that conglutinin binds fluid-phase C3b and C3c as well as iC3b. We re-investigated the reactivity of conglutinin towards fluid-phase C3 degradation products. ELISA wells were coated with conglutinin and reacted with C3 split products generated in normal human serum, in factor I-deficient serum, or in factor I-depleted serum. Conglutinin-bound C3 fragments were detected with anti-C3c and anti-C3d antibodies. An increased signal was observed during the activation of complement in normal human serum with the peak response after 1-2 hr, following which the signal decreased, reaching background level after 72 hr. The oligosaccharides on C3c, generated in serum, are thus not recognized by conglutinin. No signal was observed when factor I-deficient serum or factor I-depleted serum was used instead of normal serum. Reconstitution with purified factor I re-established the normal pattern. Examination of the conglutinin-bound C3 molecules by SDS-PAGE and Western blotting with anti-C3c and anti-C3d antibodies revealed bands characteristic for iC3b, and no bands corresponding to C3b or C3c. Reduction of the disulphide bonds prior to the incubation of the activated serum with the conglutinin-coated wells revealed a band of 63,000 MW, characteristic of the N-terminal fragment of the alpha-chain of iC3b. We also investigated the binding to the solid-phase conglutinin of purified C3 and degradation products generated with enzymes. In this case, C3 as well as C3b and C3c were bound, suggesting conformational changes in C3 during purification. In conclusion, when C3 conversion takes place at near physiological conditions, conglutinin interacts specifically with the oligosaccharide on the alpha-chain of iC3b.

Animals↗
PubMed2001

Pre-operative levels of serum immunoglobulins, circulating immune complexes and complement proteins in patients with different types of neoplasms.

In the sera of 30 neoplasm patients without metastases, the average IgG level was higher than in the control group (CG) (18.16+/-5.10 vs. 12.62+/-2.14 g/l or 12.22+/-2.14 after excluding an outier). Average concentrations of circulating immune complexes (CIC), IgM, complement 1 inhibitor (Cli), C3c and C4 did not statistically differ between the groups. Dividing the patients' group into: breast or ovary cancer (BC), melanoma (M), digestive tract cancer (DT) and other neoplasms (ON) subgroups revealed that the IgG increase did not apply to the BC group. Relatively decreased CIC concentrations in the BC and DT group and an increased Cli in the DT group were found. Several diversities detected in the humoral immunity indices' distributions and correlations suggest activation of different mechanisms depending on the neoplasm types.

Adult↗
PubMed1997

Clusterin and the terminal complement pathway synthesized by human umbilical vein endothelial cells are closely linked when detected on co-cultured agarose beads.

Clusterin and the terminal complement pathway synthesized by human umbilical vein endothelial cells are closely linked when detected on co-cultured agarose beads. Clusterin is a multifunctional regulatory protein rendering the terminal complement complex (TCC) soluble and unable to insert into cell membranes. The aim of the present study was to examine whether clusterin was an integral part of serum-derived TCC bound to agarose beads which activate the alternative pathway of complement. Further, we searched for evidence of clusterin synthesis in human umbilical vein endothelial cells (EC) and whether this synthesis was regulated by various proinflammatory cytokines (IL-1, IL-6, and TNF) and IFN-gamma. The clusterin and TCC on co-incubated beads were measured by radioimmunoassay based on primary anti-complement antibodies (anti-C3c, anti-TCC, anti-clusterin). We found that clusterin in serum experiments is bound to C9 in agarose bound TCC and not directly to the agarose. Addition of the protein synthesis inhibitor cycloheximide to cultured human umbilical vein cells resulted in a strong reduction (about 70%) of anti-clusterin binding to co-cultured beads, which strongly supports de novo synthesis of clusterin in EC. The results indicate that clusterin derived from the EC is linked with the TCC on the co-incubated beads for the following reasons: First, in serum experiments clusterin like vitronectin, was co-deposited with C9 in agarose-bound TCC. Second, cytokine stimulation of the EC with proinflammatory cytokines such as IL-1, IL-6 and TNF, known to increase the detection of bound TCC, also increased the amount of clusterin detected on the beads. Third, IFN-gamma, which reduces the concentration of bound TCC, exhibited the same effect on the amount of clusterin detected on such beads. There was a strong and dose-dependent reduction of anti-TCC binding from about 45% to about 95% when clusterin (5-40 micrograms/ml) was added to EC cultures. This effect was also evident (about 40-50% inhibition of bound TCC) using human serum as complement source. These results are probably mainly caused by clusterin binding to C5b-7, making this complex soluble without the capacity to bind to the agarose surface. This study supports the view that clusterin is a potent regulator of TCC at the levels of C5b-7 and C9.

Cells, Cultured↗
PubMed1989

Storage of platelets in earth orbit. Effect of gravity and the formulation of plastic storage containers on platelet IgG and C3.

We investigated the effects of gravitational force and three different plastic formulations of the storage bags on the quality of stored platelets by measuring the changes in platelet-associated immunoglobulin G (IgG) and two antigenic markers of the third component of human complement (C3), C3d and C3c. Pooled platelets were stored in parallel at microgravity (MG) and on the ground (1 g) using three different plastic polymers: (1) polyvinylchloride (PVC) plasticized with di-2-ethylhexyl phthalate (DEHP); (2) PVC plasticized with trioctyl trimellitate (TOTM), and (3) unplasticized polyolefin (PO). The IgG and C3 were quantified by an automated antiglobulin consumption test in freeze/thaw disrupted platelets (total IgG or C3). The baseline values for platelet associated IgG and C3, measured after 2.5 days of storage at 1 g just prior to the launch, fell within the normal range. Following an additional 6.5 day storage, platelets stored at MG had accumulated significantly less C3d than those stored at 1 g, suggesting that MG storage was beneficial. Specific plastic formulations also exerted a significant effect on the accumulation of these immunoproteins, the effect being particularly pronounced at MG. The smallest increases of IgG and C3 were seen in platelets stored in TOTM and the largest in those stored in DEHP. It is possible that further studies at MG would permit a clear characterization of the effects of other independent storage variables.

Benzoates↗
PubMed1986

Cyclophosphamide treatment in polyarteritis nodosa.

Five male patients with polyarteritis nodosa were treated with cyclophosphamide as follows: 3 mg/Kg/die i.v. up to maximum of 3 g.; subsequently, 200 mg/die per os for two weeks, then 100 mg per os every other day for three months; finally, 100 mg every fourth day until the 18th month. One patient, who also had fever, received 25 mg/die of prednisone for the initial three weeks of treatment. Before treatment ESR, WBC, and circulating immune-complexes were increased, while C3a, C3c and C4 serum complement components levels were normal. Skin ulcers healed within 4 months. A progressive marked improvement of visceral damages in the first months of therapy have been noted (e.g. blood pressure values in normal range after suspension of concomitant antihypertensive treatment, regression of peripheral neuropathy, etc. etc.). No further ischemic lesions occurred during treatment. Significant decreases of ESR and serum immune-complexes levels were detected. No untoward effects due to cyclophosphamide were observed. These findings support the effectiveness of this drug in polyarteritis. The possibility of association with glucocorticoids during the acute phase of disease is also discussed.

Adult↗
PubMed1994

Roller and centrifugal pumps compared in vitro with regard to haemolysis, granulocyte and complement activation.

A Biomedicus centrifugal pump and a Polystan roller pump were compared in vitro with regard to differences in haemolysis, granulocyte and complement activation. Six circuits of tubing and oxygenators were connected to each pump. Heparinized fresh human blood was circulated for 72 hours in the systems. Blood samples were drawn at defined intervals. Haemolysis was assessed by determination of lactate dehydrogenase (LD) and potassium, and granulocyte activation by quantification of the granulocyte proteins calprotectin, lactoferrin and myeloperoxidase. Complement activation was assessed by measuring C3 activation products (C3b, iC3b and C3c), and the terminal C5b-9 complement complex (TCC). The results indicate more haemolysis and complement activation in the roller pump group, revealed by significantly higher concentrations of LD, potassium, C3 activation products and TCC. Calprotectin, lactoferrin and myeloperoxidase were all significantly increased in both groups, but the rise appeared earlier in the roller pump group. The concentrations of LD and potassium both correlated significantly with C3 activation products, indicating that complement activation may at least partly be responsible for the haemolysis.

Cell Adhesion Molecules, Neuronal↗
PubMed1997

Imaging of the Early Events of Classical Complement Activation Using Antibodies and Atomic Force Microscopy

In the present report we use atomic force microscopy (AFM) combined with antibody techniques to study the lateral distribution of specific serum proteins adsorbed onto flat silicon surfaces precoated with immunoglobulin G (IgG). Null-ellipsometry was used as a complimentary technique to quantify the adsorbed protein layers. After 15 s of incubation in human blood serum a partial monolayer of randomly distributed serum proteins was observed. The following exposure to antibodies to complement factor 1q (anti-C1q) resulted in a development of enlarged protein aggregates and a significant increase in adsorbed mass. Conversely, exposure to antibodies to complement factor 3c (anti-C3c) resulted in only a few randomly distributed protein aggregates and a much smaller increase in adsorbed mass. After 60 s of serum incubation the entire surface was covered with a proteinaceous film with irregular topography. This layer bound large amounts of anti-C3c but showed significantly smaller affinity for anti-C1q. Prolonging the serum incubation to 30 min resulted in an increased thickness and roughness of the protein layer and caused a massive deposition of anti-C3c but no anti-C1q. The results suggests that the transient affinity of anti-C1q, seen on various classically complement activating surfaces, is due to a shielding of the initially adsorbed proteins by subsequently deposited layers of C3. The results also show that qualitative information of the lateral organisation of specific proteins in a heterogeneous mixture can be assessed using AFM in combination with immunological techniques.

Journal Article↗
PubMed1985

High levels of C3c in the cerebrospinal fluid from amyotrophic lateral sclerosis patients.

A study of several parameters of the humoral immunity in the serum and the cerebrospinal fluid (CSF) of thirteen Amyotrophic Lateral Sclerosis (ALS) patients was carried out. A significant increase in CSF C3c was shown. This feature was found to be significantly correlated to the CSF albumin/serum albumin ration (r = 0.70; p less than 0.05) and to the total CSF proteins (r = 0.86; p less than 0.01). The possible effect of the blood-brain barrier breakdown on the CSF complement levels was evaluated. On the basis of the recently found biochemical changes in ALS cell membranes it is proposed that the high levels of the CSF C3c may also be due to a defective binding to the lymphocytes C3 receptors.

Adult↗
PubMed1998

Extracorporeal ("ex vivo") connection of pig kidneys to humans. III. Studies of plasma complement activation and complement deposition in the kidney tissue.

The complement system is one of the important factors involved in the hyperacute rejection of xenografts. This report deals with the activation of the complement system in a clinical trial where pig kidneys were extracorporeally connected to two volunteer dialysis patients who were pretreated with plasmapheresis in order to substantially reduce anti-pig xenoantibodies. The clinical data of the perfusion experiments and the patients humoral immune response to pig xenoantigens have been reported in detail (Xenotransplantation 1996; 3:328-339, 340-353). Three consecutive daily plasmapheresis treatments of the patients reduced the plasma complement protein (C3, C4, and C5) concentrations to 8-27% of the baseline values. The perfusion of the pig kidney connected to patient 1 was terminated at 65 min due to graft rejection and this patient was not hemodynamically affected by the experiment. The second experiment was terminated at 15 min due to an anaphylactic like reaction of the patient. In patient 1 a slight reduction of plasma C3, C4, and C5 and an increase of C5a and SC5b-9 occurred, while C3a decreased during the perfusion. Patient 2 had an increase of all complement parameters, most prominent for C4d and SC5b-9, which occurred concomitant with the appearance of the anaphylactic like side effects. In general, plasma levels of PMN elastase, IL6 and IL8 increased in both patients during the perfusion. Immunohistochemical investigation of the kidney tissues revealed deposition of human complement factors C1q, C4c, and C3c in a congruent pattern with the vasculature of the kidney in patient 1. In kidney 2 only trace amounts of C1q and C3c were found. Both kidneys were negative for properdin. Therefore, in this experimental set up with extracorporeal connection of pig kidneys to the human circulation the human complement cascade is activated mainly through the classical pathway.

Adult↗
PubMed2003

Molecular characterization of the pig C3 gene and its association with complement activity.

The complement system catalyzes direct lysis of micro-organisms and modulates phagocytosis, inflammation, humoral and cellular immune responses. Since the complement protein C3 is the central component within all pathways of complement activation, C3 is a candidate gene for complement activity and also for improved protection against many pathogens. The pig C3 gene was sequenced, screened for polymorphisms, and analyzed for association with hemolytic complement activity of the alternative and classical pathway (AH(50), CH(50)). C3c serum levels and haptoglobin (HP) serum concentrations were measured before and after vaccination against Mycoplasma hyopneumoniae, Aujeszky virus, and porcine reproductive and respiratory syndrome virus in F2 animals of a pig resource population based on crossbreeding of Duroc and Berlin Miniature Pig. The genomic C3 sequence covers 444 bp of promoter region, 41 exons and 40 introns, as well as 881 bp of the 3'-flanking region. The cDNA codes for a 1,661-amino acid precursor C3. Five polymorphic sites were detected in the 5'-UTR, intron 13, exon 15, exon 30, and the 3'-UTR. Within the resource population two haplotypes were found to segregate. Analysis of variance applying a repeated measures model revealed a significant effect of the interaction of C3 genotype and time of measurement relative to immunization on CH(50), AH(50,)and C3c that is likely to be due to variation of C3 expression. In contrast, the time course of the HP acute-phase reaction is not associated with C3 genomic variation. The association of C3 with complement activity indicates the importance of C3 as a candidate gene for natural resistance to micro-organisms, although the causative polymorphism modulating the expression of C3 remains to be delineated.

Alleles↗
PubMed1980

Numerical changes in T cell subsets (T gamma and T mu) in leprosy patients.

Eighty-six leprosy patients (49 active lepromatous, 24 inactive lepromatous 7 borderline, and 6 tuberculoid) and nine healthy controls were examined for numerical changes in T cell subsets (T gamma and T mu), and complement levels in peripheral blood to determine the roles of T cell subsets and complement in the etiology of leprosy. The percentage and number of T gamma and T mu showed no significant differences among the different clinical groups, but 4 out of 49 active lepromatous, 3 out of 24 inactive lepromatous and 3 out of 7 borderline cases showed a high prcentage of T gamma cells. Serum concentrations of C4, C3c, and C3 activator, an important factor in the alternative pathway of complement activation, were not significantly different among the groups. However, C3 activator and C3c concentrations were significantly high in active lepromatous patients complicated by an immune complex disease called "erythema nodosum leprosum" (ENL) compared with ENL-free active lepromatous leprosy.

Adult↗
PubMed2000

Complement activation in SCID and nude mice is related to severity of tissue inflammation in the Candida mastitis model.

A small animal model of localised candidiasis is needed for the evaluation of new antifungal compounds. Mammary glands of immunocompetent (BALB/cJ) and immunodeficient (SCID and athymic nude) mice were infected with a wild-type of Candida albicans. Some of the animals were treated with amphotericin B (AmB) while others were treated with saline and acted as controls. The histologic changes of infected mammary gland tissues and a number of other organs were evaluated. Complement (C) activation was analysed by immunoelectrophoretic quantification of molecules with C3c epitopes (C3, C3b, iC3b, and C3c) in serum. In all animals the organisms were confined to the mammary glands. Serum C3c levels were significantly higher (P<0.05) in infected untreated BALB/cJ and SCID mice, which also had severe mammary gland tissue inflammation, compared with control mice treated with AmB (4 mg kg(-1) i.p. once daily for 4 days). Both treated and control nude mice showed less tissue inflammation compared to BALB/cJ and SCID mice, and revealed insignificant activation of the complement system. It is concluded that innate immune response is important in the control of candidiasis and that the murine mastitis model is useful for immunopathological studies as well as evaluation of potential antifungal compounds.

Amphotericin B↗
PubMedDate not supplied

The significance of red cell bound complement components in development of standards and quality assurance for the anti-complement components of antiglobulin sera.

Human red blood cells, sensitized with complement in vivo and by a variety of methods in vitro, (e.g. blood group antibody, low ionic strength, alternate pathway), were tested with a battery of anti-complement sera (anti-C3, -C3c, -C3d, -C4, -C4c). Red blood cells could be prepared by relatively simple methods to yield cells sensitized with C3 and C4, C3 but not C4, C4 but no C3, C3d with no C3c and C4d with no C4c. These cells are suitable for standarization and quality assurance of antiglobulin sera (AGS). Anti-C3d is necessary for optimal detection of sensitization of red blood cells by complement in vivo by the direct anti-globulin test (DAT). Anti-C3d may also be optimal for the indirect antiglobulin test (IAT) especially if incubation periods greater than one hour are employed. Potent anti-C4 and anti-C3 antisera made in the authors' laboratory resulted in numerous weakly positive antiglobulin tests when testing red blood cells from refrigerated clots (especially anti-C4) but red blood cells from refrigerated anticoagulated segments gave negative results. When red blood cells were incubated in normal serum at room temperature (as in the room temperature phase of a compatibility test), some positive results were again obtained with the potent anti-C4 and anti-C3 antisera. However, one commercial antiglobulin serum containing anti-complement antibodies that were at least as potent as any other commercial antiglobulin serum gave uniformly negative results under the above conditions. Anti-C4 antibodies may be omitted from anti-globulin sera without decreasing the efficacy of such antisera to be used in compatibility testing. Thus, positive results in the compatibility test due to detection of clinically insignificant cold antibodies in the IAT by the anti-complement antibodies in AGS, may be avoided if anti-C4 is omitted or is in low concentration and if the concentration of anti-C3d is carefully standardized. A higher concentration of anti-C3d could be used for compatibility tests if red blood cells from anticoagulated segments were used instead of those from clots and if a separate tube were used for the IAT at 37 C rather than using one tube for both room temperature and 37 C incubations.

Antibody Specificity↗
PubMed1984

Role of C3 in the control of monocyte C2 production.

Serum-treated antigen-antibody complexes (IC) and DTSP-polymerized C3b and C3c inhibited the production of the second complement component (C2) by monocytes in culture, whereas monomeric C3, C3b, C3bi, C3c or C3d had no effect. The degree of inhibition of dithiobissuccinimidyl propionate (DTSP)-polymerized C3 was proportional to the degree of polymerization, dimer exhibiting less inhibitory activity than larger molecular weight polymers. The inhibitory effect of serum-treated IC and DTSP-polymerized C3b was abrogated by their pretreatment with Fab fragments of anti-C3, or pretreatment of monocytes with Fab fragments of antiserum to the C3b receptor (CR1). We have concluded that the inhibition of C2 production produced by serum-treated IC is due to bound C3b or C3bi, and is mediated by CR1. Furthermore cross linking of receptors is required for this effect; two or more than two receptors must be cross-linked for a significant effect to be observed.

Antigen-Antibody Complex↗
PubMed1996

Beneficial effects of systemic immunoglobulin in experimental membranous nephropathy.

To test the hypothesis that systemic administration of immunoglobulin might reduce glomerular injury in membranous nephropathy through mechanisms involving inhibition of complement activation, we studied the passive Heymann nephritis (PHN) model of membranous nephropathy in rats. The daily administration of immunoglobulin goat IgG (600 mg/kg i.p.) reduced proteinuria by 52%. Quantitative immunohistochemical analysis showed that the glomerular deposition of C3c, an indicator of ongoing complement attack, and of C5b-9 was significantly decreased in the immunoglobulin treated group, while deposition of anti-Fx1A was not affected. Electron microscopic analysis demonstrated that the extent of subepithelial immune complexes did not appreciably differ between treated and control animals. Systemic complement levels were not altered by immunoglobulin treatment. These data suggest that the reduction in proteinuria that resulted from systemic immunoglobulin administration was mediated by modifying the effect of complement induced glomerular injury. This interpretation was further supported by in vitro data that documented a significant reduction in C5b-9 induced glomerular epithelial cell lysis in the presence of both goat and rat IgG. These results indicate that systemic administration of immunoglobulin can substantially reduce ongoing complement activation in the glomerulus in PHN rats and that this effect is associated with a significant reduction in glomerular injury.

Animals↗
PubMed2003

Aggregation of human platelets in plasma by porcine blood cells in vitro is probably mediated by thrombin generation.

The infusion of pig progenitor cells into baboons is associated with a thrombotic microangiopathy probably related to the interaction of these cells with the baboon endothelial cells and platelets. We have shown previously that pig peripheral blood mononuclear cells (p-PBMC), are able to activate the human coagulation cascade as they are able to generate thrombin when added to defibrinated plasma. In this work, we have tested the interaction of p-PBMC with human platelets to assess the capacity of p-PBMC to cause platelet aggregation and the possible role of complement activation in this aggregation. Human platelet aggregation assays, using collagen (1 or 2 microg/ml), were performed with platelets in platelet-rich plasma (PRP) or platelets washed by filtration. PRP or washed platelets were also incubated with p-PBMC or human PBMC (h-PBMC) at several concentrations and aggregation was measured. The effect of Dansylarginine N-(3-ethyl-1,5-pentanediyl)amide (DAPA), an inhibitor of thrombin, was studied on platelet aggregation caused by the pig cells. Complement activation was measured by deposition of fragment c derived from C3 splitting (C3c) on pig cells incubated with citrated platelet poor plasma (PPP). When human PRP was incubated with p-PBMC, aggregation was a consistent event quantitatively similar to that induced by collagen. No aggregation of washed platelets was observed when these were incubated with p-PBMC or h-PBMC. Aggregation of human platelets in PRP, induced by p-PBMC, was inhibited when DAPA (100 microm) was added to the incubation mixture (23%), indicating that the thrombin inhibitor blocked the capacity of p-PBMC to aggregate human platelets. No deposition of C3c fragments on p-PBMC was detected when the porcine cells were incubated for up to 20 min with citrated PPP. The fact is that p-PBMC induces human platelet aggregation in plasma being thrombin generation a likely explanation for this observation. Our data suggest that, in the system assayed, complement activation is not a cause of platelet aggregation. These findings are relevant for the clarification of the reported thrombotic microangiopathy complicating the intravenous infusion of pig cells in primates in attempts to induce pig tolerance in baboons.

Animals↗
PubMed1983

An evaluation of nephelometry and complement-based tests for the detection of circulating immune complexes.

Sera from 20 normal adult control subjects and 28 patients suffering from various diseases which may be associated with an immune complex disorder were investigated, using three different techniques for detection of circulating immune complexes (CICs). The sera from the patients were assigned expected positive or negative ratings by the clinicians according to clinical and laboratory criteria. This information as well as the diagnoses was withheld until the results of immune complex determinations were available. The three tests used to detect CICs were laser nephelometry (LN), 125I-C1q binding and measurement of the C3 breakdown product C3c. Serum levels of the complement components C3 and C4 were assessed on the serum specimens from the patients. Results obtained from normal control sera showed that 18 of the 20 and all 20 were negative with the C1q binding technique and LN respectively. Of 16 sera for which a positive result was expected, 5 (31,3%) and 14 (87%) were positive when examined by the C1q binding technique and LN respectively; C3c determination produced no positive results. No false-negative results were obtained with the C1q binding and C3c tests, but 2 out of 16 (13%) results obtained with the LN test were false negative. LN is a rapid, sensitive test for the detection of CICs.

Antigen-Antibody Complex↗