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PubMed1990

Enhanced Ig production by human peripheral lymphocytes induced by aggregated C1q.

Because B cells express receptors for C1q, we have investigated the role of C1q in the stimulation of B cells. When B cells were cultured in the presence of C1q that had been frozen, T cells, and suboptimal concentrations of PWM, there was a dose-dependent enhancement of IgM, IgG, and IgA by the B cells. No significant enhancement of Ig production by B cells was seen in the absence of T cells or PWM. The contribution of T cells or PWM could be replaced by supernatants of PMA and Con A-activated PBMC (T cell growth factor). C1q that had been frozen, in contrast with freshly isolated C1q, was at least 3 times more active in enhancement of the production of Ig by B cells in culture in the presence of suboptimal concentrations of T cell growth factor. The capability of C1q to stimulate B cells could be ascribed to aggregates of C1q. Monomeric C1q was only marginally active to stimulate B cell Ig production, whereas dimeric and tetrameric C1q were able to enhance Ig production by B cells in relation to their size. Furthermore, aggregation of C1q on soluble aggregates of rabbit IgM also increased its potential to enhance B cell Ig production. The interaction of C1q with the B cells occurs via the collagenous tail of C1q, as suggested by inhibition experiments with purified collagenous tails and globular heads of C1q. These results indicate that triggering of C1qR on B cells positively regulates Ig production in vitro.

Antibody Formation↗
PubMed1990

Interaction of C1q with its receptor on cultured cell lines induces an anti-proliferative response.

The receptor for human C1q (C1qR) is expressed on a wide variety of somatic cells, including cultured cell lines of different lineages such as Raji, Daudi, Wil2WT, U937, and Molt4. In this report, we present evidence which shows that culturing of C1qR-expressing cell lines with C1q inhibits their growth. When each of the different cell lines were cultured for 5 days with or without various concentrations (5-50 micrograms/ml) of micro-filtered (0.22 micron) C1q, cell proliferation was inhibited in a dose-dependent manner with maximal inhibition (90%) occurring at a concentration of 50 micrograms/ml at Day 4 of culture. This anti-proliferative effect of C1q was inhibited when 30 micrograms/ml of F(ab')2 anti-C1q was included in the culture with C1q while the antibody alone did not have any effect. The specificity of this interaction was further substantiated by the finding that neither macromolecular C1, or subcomponents C1r and C1s, nor human or murine IgG nor IgM had any inhibitory activity when cultured with these cell lines. That this C1q-induced inhibition of cell growth is mediated by C1qR was deduced from experiments in which (i) culturing of cells in the presence of two IgM monoclonal antibodies II1/D1 and II1/B5, directed against the C1q-binding site of C1qR resulted in the inhibition of cell growth while nonimmune murine IgM did not, and (ii) the collagenous portion of C1q (c-C1q) which contains the intact, C1qR-binding domain was also capable of inhibiting cell proliferation in a manner similar to intact C1q. The effect of C1q was not cytotoxic but cytostatic since the number of dead cells in the C1q-treated cultures was not significantly different than that in the untreated cells (5% vs 4%), a figure which represents the normal wear and tear of tissue culture conditions. On the basis of these findings we propose that the C1qR alone or in conjunction with other cellular factors may function as a molecule which supports cell growth. Upon ligand binding, however, the ligand-receptor interaction may suppress postreceptor events which are necessary for cell proliferation.

Carrier Proteins↗
PubMed1984

Interaction of C1q with beta 2-microglobulin.

Beta 2-microglobulin aggregated with glutaric dialdehyde was efficiently bound to C1q in fluid and solid phase assay systems. Furthermore, affinity chromatography experiments suggested reactivity of monomeric beta 2-microglobulin with C1q. In spite of its C1q binding capacity, the aggregated beta 2-microglobulin did not activate the C1 complex in serum. This however, might have been due to the mode of aggregation.

Binding Sites↗
PubMed1996

The complement system is defective in chronic lymphatic leukemia patients and in their healthy relatives.

The present study was aimed at analyzing the existence of an impaired complement system in CLL patients. For this purpose, the serum levels of the serum complement proteins C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, C9, Factor B and properdin were repeatedly evaluated by means of radial immunodiffusion assay in 26 CLL patients over a period of 2 years. At the time of diagnosis, 18 of the 26 CLL patients showed low serum levels in at least one of these complement proteins as compared to a group of sex- and age-matched healthy subjects (P < 0.0001). Complement defects affected either the classical and/or the alternative pathway components, and in some case low levels of late components (C5-C9) were also observed. A reduced level of properdin was the most frequent abnormality (11/18). The presence of such abnormalities were correlated with the stage of the disease, and they were found in 100% of the patients (11) in advanced stages (Rai II-IV), and in 40% of patients (15) in early stages (0-1) (P < 0.004). Severe infections occurred in five patients; four of them were in advanced stages of the disease and had decreased levels of at least one complement component, whereas the remaining patient was in an early stage and had normal levels of complement components. These data support the notion that an impaired complement system might be involved in the pathophysiology of CLL and its infectious complications. Although more work is needed to sustain this hypothesis, we discuss the possibility on the basis of data obtained in the first-degree relatives of CLL patients, that in some CLL patients the complement deficit might reflect a genetic predisposition.

Adult↗
PubMed1997

Deposition of antibodies to the collagen-like region of C1q in renal glomeruli of patients with proliferative lupus glomerulonephritis.

OBJECTIVE: To determine if antibodies to the collagen-like region of C1q (C1q-CLR) are present in the glomerular immune deposits of patients with systemic lupus erythematosus (SLE). METHODS: Kidney tissues were obtained at autopsy, glomeruli were isolated, and glomerular basement membrane fragments were prepared. Antibodies were extracted with low pH or with DNase. RESULTS: The concentrations of antibodies to C1q-CLR recovered from the glomeruli were > or =50-fold higher per unit of IgG than that found in the serum or in the serum and interstitial fluid entrained in glomeruli. Antibodies to C1q-CLR were recovered from glomeruli of 4 of 5 patients with proliferative glomerulonephritis at autopsy. CONCLUSION: This is the first demonstration that antibodies to C1q-CLR are deposited and concentrated in the renal glomeruli of patients with SLE. These antibodies, thus, have the potential of contributing to the pathogenesis of lupus glomerulonephritis.

Antibodies↗
PubMed1984

The effects of cleavage of the inter-chain disulphide bonds of rabbit IgG on its ability to bind C1q.

Immune complexes prepared from rabbit anti-ovalbumin IgG in which the interchain disulphide bonds had been reduced and then blocked with N-( iodoacetylaminoethyl )-8-naphthylamine-1-sulphonic acid retained the ability to bind 125I-labelled C1q. This ability was lost when a small alkylating agent (iodoacetamide) was used to block the cleaved disulphide bonds. The ability of the IgG to form insoluble immune complexes was partially compromised when iodoacetamide was used to block the disulphide bonds, but was unimpaired when N-( iodoacetylaminoethyl )-8-naphthylamine-1-sulphonic acid was used. These data are consistent with the suggestion that access to the C1q binding site in IgG in immune complexes is modulated by movement of the Fab arms, which may block access to the site.

Antigen-Antibody Complex↗
PubMed1989

[Use of solid-phase Clq-ELISA for detecting circulating immune complexes in human diseases].

The authors provide the results of studying the methodologic characteristics and of the clinical trial of the C1q-ELISA for detection of the circulating immune complexes. The C1q-ELISA is shown to have a high sensitivity and to make it possible to identify 3 micrograms/ml and more of aggregated gamma-globulin. The method can use for detection of CIC E (ab')2-fragments of antibodies to IgG of man and protein A labeled with peroxidase. Using the method, the circulating immune complexes were identified in the sera of 50% of patients with systemic lupus erythematosus, of 30% of patients with dilated cardiomyopathy and of 53% of patients with nonspecific aortoarteritis. It is concluded that the C1q-ELISA can be used in clinical practice for detecting the circulating immune complexes in different diseases of man.

Antigen-Antibody Complex↗
PubMed1990

IgG and IgA antibodies to the collagen-like region of C1q in rheumatoid vasculitis.

We investigated the presence of IgG and IgA antibodies to C1q in serum samples from 80 patients with rheumatoid arthritis (RA), 31 patients with rheumatoid vasculitis, and 80 healthy controls. IgG and IgA antibodies to C1q, as measured by enzyme-linked immunosorbent assay, were found in less than 5% of the sera from RA patients and from healthy controls. In contrast, IgG and IgA antibodies to C1q were found in 29% and 61%, respectively, of the sera from patients with rheumatoid vasculitis. The occurrence of IgA antibodies to C1q has not been previously demonstrated. These results also demonstrate that IgG antibodies to C1q do not occur exclusively in systemic lupus erythematosus patients: Sera of patients with rheumatoid vasculitis frequently contain IgG or IgA antibodies to C1q, which contribute to immune complex formation.

Adult↗
PubMed1986

Rubella-associated arthritis. II. Relationship between circulating immune complex levels and joint manifestations.

The role played by raised circulating immune complex (CIC) levels in the pathogenesis of rubella-associated joint reactions has been assessed during the course of RA 27/3 rubella immunisation and epidemic wild rubella infection. CIC levels were evaluated by C1q microplate enzyme-linked immunosorbent assay (ELISA) and Raji cell ELISA techniques. Mean CIC levels were generally higher both before and after immunisation among individuals developing vaccine-associated arthritis than among those developing arthralgia or no joint symptoms. However, these differences reached statistical significance only with CIC (Raji) techniques at six and 12 weeks postimmunisation. The proportion of individuals within each group having raised CIC levels (greater than or equal to 2SD above normal control values) was also higher in the postvaccine arthritis group, though statistically significant differences were not found with either Raji or C1q techniques. These data do not support a direct role for raised CIC levels in the pathogenesis of rubella-associated arthritis or arthralgia.

Antigen-Antibody Complex↗
PubMed1988

Inhibition of C1q functions by RHP, a protein elevated in sera from patients with rheumatoid arthritis.

We have previously shown that serum levels of C1q, unbound to C1r X C1s, are elevated in rheumatoid arthritis. We have also shown that RHP, a newly described serum protein which affects the C1q-anti C1q precipitin reaction, is also present at elevated levels in rheumatoid arthritis. We now show that RHP inhibits the hemolytic activity of C1q, disaggregates C1, and inhibits the ability of C1q bound to latex beads or to aggregated IgG to enhance the oxidative metabolism of neutrophils.

Adsorption↗
PubMed1999

Anti-C1q antibody as a marker of disease activity in systemic lupus erythematosus.

The present study was conducted to examine the usefulness of anti-C1q antibody as a marker of disease activity in Indian patients with systemic lupus erythematosus (SLE). We standardized the assay for detection of IgG anti-C1q antibody using ELISA. The normal cut-off level was determined by testing 57 healthy, age and sex matched controls to be 53 units/m1 (mean +/- 2 SD). Patients with SEL (97 females and 13 males) were studied and the following parameters were obtained on all: SLE disease activity index (SLEDAI), anti-C1q, anti-ds DNA and C3. Correlations were tested between these parameters using Spearman's rank correlation coefficients. Anti-C1q was found positive in 66 (60%) patients while anti-ds DNA was found in 78 (71%). The positive predictive values of anti-C1q and anti-ds DNA for lupus nephritis were 59 and 61 per cent respectively. The titres of anti-C1q correlated positively with SLEDAI (P < 0.01) and anti-ds DNA (P < 0.01) and negatively with C3 levels (P < 0.001). No significant correlation was observed between anti-C1q positivity and any particular organ involvement. Similarly, no correlation was found between anti-C1q and proliferative lupus nephritis. Anti-C1q was found positive in 5 of 9 patients with moderate SLEDAI scores and negative for anti-ds DNA antibody. It is concluded that anti-C1q antibody can serve as a general marker for lupus activity, supplementing the currently used serum markers.

Adolescent↗
PubMed1985

Low molecular weight C1q in systemic lupus erythematosus.

In sera of patients suffering from an exacerbation of systemic lupus erythematosus (SLE), increased amounts of abnormal C1q were detected, contrasting with decreased or even undetectable levels of normal C1q in these sera. When analyzed immunochemically by double immunodiffusion, this low m.w. C1q (LMW-C1q) appeared to be identical with the defective C1q in serum of individuals with an inherited, homozygous inability to produce functional plasma C1q. These persons show a tendency to develop SLE-like syndromes. Like the genetically defective C1q, the abnormal C1q molecule in SLE sera was hemolytically inactive, did not incorporate in C1, was found in the supernatant of euglobulin-precipitated serum, and appeared in the break-through fraction of a cation-exchange column. Sucrose gradients and gel filtration analyses supported the putative identity of the molecules. SDS-PAGE and immunoblots revealed the presence of subunits that reacted with antibodies against C1q and confirmed the C1q-like nature of LMW-C1q. Low levels of LMW-C1q were also detected in serum and plasma of normal individuals. A radial immunodiffusion technique was used to measure LMW-C1q in the serum of 54 patients. Although these patients were not selected for parameters of disease activity, their levels of LMW-C1q were significantly higher than those of normal individuals and children with decreased C3 levels due to acute glomerulonephritis.

Centrifugation, Density Gradient↗
PubMed1983

The correlation between insulin antibodies and circulating immune complexes in diabetics with and without microangiopathy.

The relationship between immune complexes and insulin antibodies was evaluated in 237 insulin treated subjects with a duration of diabetes of more than 1 year. Ninety-seven diabetics were selected at random (group 1) whereas 140 according to the presence of diabetic microangiopathy (group 2). Immune complexes were evaluated by the solid phase C1q binding test in all patients and by conglutinin radioimmune assay in most of them. Insulin antibodies were determined by Christiansen's and Anderson's methods. Immune complexes as detected by the solid phase C1q method were found increased in group 1 and there was an inverse correlation between these complexes and insulin antibody levels. In group 2 patients with microangiopathy the amount of this kind of complex was significantly greater than in those without microvascular lesions and there was no correlation with insulin antibodies. Immune complexes as detected by conglutinin were found increased in group 2 patients and these were significantly correlated with the level of insulin antibodies. No increase in these immune complexes was found in patients with microangiopathy when compared with patients without microangiopathy. Insulin antibodies were not correlated with the presence of complications. Overall, immune complexes detected by C1q binding were significantly correlated with the presence of microangiopathy. In patients with high insulin antibody levels the complexes formed were not detected by C1q binding. The immune complexes detected by conglutinin are correlated with insulin antibodies, but not with the presence of microangiopathy.

Adolescent↗
PubMed1995

Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.

Isolated BALB/c mouse thioglycollate-elicited (inflammatory) peritoneal macrophages release at least 10 times more C1q than do isolated resident peritoneal macrophages. Addition of non-steroidal anti-inflammatory drugs (NSAID) to thioglycollate-elicited macrophages in culture inhibited the release of C1q and reduced levels of C1q-specific mRNA. Contrastingly, the NSAID were found to enhance C1q-specific mRNA levels in resident macrophages, although no increase in C1q levels secreted was observed. This suggests that the response of macrophages to NSAID, with respect to C1q synthesis, reflects the developmental stage of the macrophage. The gold salt auranofin (AFN) was found to enhance markedly C1q synthesis at both transcriptional and secretory levels in thioglycollate-elicited macrophages whilst, conversely, AFN reduced mRNA levels in resident macrophages. This indicates that AFN and the NSAID may work via the same or similar biochemical pathway, but with opposing effects. The glucocorticoid hydrocortisone (HC) greatly enhanced C1q-specific mRNA levels in both thioglycollate-elicited and resident macrophages, although no parallel increases in C1q secreted were observed. The data on inhibition of C1q biosynthesis by NSAID in thioglycollate-elicited macrophages are supported by the enhancement of C1q biosynthesis following addition of prostaglandin E2 (PGE2) or dibutyryl cyclic AMP (dBcAMP) to the cultures. From these experiments, it is concluded that C1q biosynthesis is controlled, at least in part, by a pathway involving cAMP.

Adenylyl Cyclases↗
PubMed1991

Localisation of complement components in association with glomerular extracellular particles in various renal diseases.

Intraglomerular extracellular microparticles including so-called virus-like particles and striated membranous structures have been observed in various renal diseases. The presence and localisation of complement components in these extracellular bodies was studied using the protein A-gold electron microscopy method. Ultrastructurally these particles were differentiated into microspherical structures (MSS) and thread-like structures (TS). Both structures showed weak to moderate diffuse labelling with C1s, whilst the intense labelling found with C3d and C9 was confined to individual membrane-like structures of both MSS and TS. Labelling with IgA, IgG, fibrinogen and the complement components C1q, C1r, C3c C4 and C5 showed negative or trace results. There were no differences between the immunolabelling patterns of MSS and TS, nor among different renal diseases in which these structures were found. These findings raise the possibility that formation of so-called virus-like particles such as MSS and TS may be associated with complement activation.

Complement System Proteins↗
PubMed2002

C1q nephropathy: a case with severe atopic dermatitis.

A 9-year-old boy with nephrotic syndrome who had a history of atopic dermatitis since 5 years of age is presented in this report. Generalized edema and hyperpigmented and desquamated pruritic lesions were detected on the trunk and extremities. Mesangial C1q deposition was seen on kidney biopsy. A high serum IgE level was also detected. Complete remission was achieved with steroid therapy.

Child↗
PubMed1982

125I-C1q binding activity of soluble antigen-antibody complexes formed in vitro.

The ability of the 125I-C1q binding test to detect soluble antigen-antibody complexes formed in vitro was tested with two antigen-antibody systems. Using tetanus toxoid:anti-toxoid complexes, all of the increased 125I-C1q binding activity was due to soluble immunoglobulin aggregates present in the unheated tetanus immune globulin. Using BSA:anti-BSA complexes, maximum 125I-C1q binding activity was present in the soluble supernatants from the equivalence zone. No immune complexes were present in these supernatants and the increased activity appeared to be due to alterations in endogenous C1 during the formation of large, insoluble immune complexes. The 125I-C1q binding test readily detected large, insoluble BSA:anti-BSA complexes but may not detect small, soluble complexes which have been suggested to be important in disease pathogenesis.

Antigen-Antibody Complex↗
PubMed1975

[Value of post-operative parenteral nutrition as shown by various plasma protein measurements (author's transl)].

A significant improvement in urea nitrogen and plasma protein metabolism during the first 10 days after abdominal surgery was obtained in 24 patients who received parenteral carbohydrates combined with essential amino acids and histidine. A control group of 15 patients who only received water and electrolyte balance in the post-operative phase showed significantly worse results. The observation that immunoglobulins (IgG) and complement components (C1q, C3 activator) recovered more quickly from the stress of surgery under the influence of parenteral nutrition seems to be particularly important.

Adult↗