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PubMed1993

Recurrent angioedema and urticaria.

The case reported here illustrates the life-threatening aspects of angioedema and the need to thoroughly investigate the possible causes of this clinical finding. As discussed, the causes of angioedema are numerous. Commonly implicated in drug-induced angioedema are antihypertensive ACE inhibitor drugs, as was originally thought with this patient. Because of her skin lesions and macrocytic anemia, further studies were done. These studies led to a diagnosis of hypocomplementemic urticarial vasculitis syndrome, an uncommon to rare form of acquired angioedema, urticarial vasculitis, arthritis, and obstructive airway disease associated with the production of autoantibodies to C1q. It is an autoimmune disorder related to but separate from SLE.

Angioedema↗
PubMed2006

Human serum amyloid P component binds to peripheral blood monocytes.

The binding of human serum amyloid P component (SAP) to blood cells and monocyte-derived dendritic cells was investigated by flow cytometry. Monocytes bound biotinylated SAP with avidity in a dose-dependent and saturable manner. By contrast, the binding of SAP to monocyte-derived dendritic cells was weak. No binding to erythrocytes, NK cells, T lymphocytes or B lymphocytes could be detected. The SAP-monocyte interaction was calcium-independent and readily inhibited by C1q. SAP was nonmitogenic for human mononuclear cells and had no apparent influence on lymphocyte proliferation induced by mitogenic lectins. We speculate that binding of SAP by monocytes could be of physiological relevance at extravascular sites by influencing complement regulation.

Biotinylation↗
PubMed1986

Receptor-mediated binding of C1q on pulmonary endothelial cells.

Normal undamaged pulmonary endothelial cells appear to be immunologically privileged in that they do not express receptors for the Fc portion of IgG nor for C3b. However, these receptors become unmasked on endothelial cells injured by viral infection or exposure to white cell lysates. We now present evidence to indicate that C1q binds to specific receptors on the surface of normal healthy endothelial cells. The binding is dose-dependent, reversible and saturable. Furthermore our data show that binding of C1q to endothelial cells is via the collagenous portion of the molecule not via the globular head regions. Thus binding of C1q to endothelium would have the effect of exposing Fc receptors that could then bind to IgG of circulating immune complexes. That Fc receptors are in fact exposed is shown by rosette formation with antibody sensitized erythrocytes. With 2C1r-2C1s-associated C1q, no binding occurred using C1 fixation and transfer assays. Our results indicate that C1q binding to endothelium provides a means for localizing immune complexes on pulmonary vessels and may be important in the initiation and progression of the inflammatory response.

Animals↗
PubMed2003

Immune deposition of C1q and anti-C1q antibodies in the kidney is dependent on the presence of glomerular IgG.

Anti-C1q autoantibodies are found frequently in patients with Systemic Lupus Erythematosus (SLE) and several studies indicate that these autoantibodies are associated with renal involvement. We have shown earlier that administration of anti-C1q antibodies to normal BALB/c mice results in the deposition of these antibodies and C1q in the kidney. In the present study we have investigated which factors are essential for this C1q-anti-C1q deposition. Injection of anti-C1q antibodies in C57BL/6 mice results in deposition of both C1q and anti-C1q in glomeruli, while administration of equal concentrations of anti-C1q to immunoglobulin deficient Rag2-/- mice did not result in deposition of anti-C1q antibodies. Analysis of renal sections of naive Rag2-/- mice revealed absence of mouse IgG and C1q in the glomeruli, while circulating C1q was within normal levels. Reconstitution of Rag2-/- mice with IgG, either by injection with purified mouse IgG or by splenocyte transfer, resulted in restored localization of mouse IgG together with C1q in the kidney. Subsequent injection of anti-C1q antibodies in these IgG reconstituted mice resulted in clear deposition of C1q together with anti-C1q in the kidneys comparable to that found in C57BL/6 mice receiving anti-C1q. We propose that the continuous presence of serum derived non-immune IgG in the glomerulus serves as a target for low affinity interactions with C1q, which then can serve as antigen for anti-C1q antibodies. Therefore we hypothesize that high and fluctuating levels of IgG as observed in patients with SLE may contribute to flares of renal inflammation in those patients with anti-C1q autoantibodies.

Animals↗
PubMed2006

Clinicopathologic correlation of C1q nephropathy in children.

BACKGROUND: Clinicopathologic correlation of C1q nephropathy is clarified poorly. The aim of our study is to clarify clinicopathologic correlation in childhood C1q nephropathy. METHODS: Thirty children aged 3 to 15 years who met criteria proposed by Jennette and Hipp were enrolled in this study. RESULTS: According to their presentation at onset, children were divided into 2 groups: the asymptomatic urinary abnormalities (asymptomatic) group (n = 18) and the nephrotic syndrome (NS) group (n = 12). Light microscopy showed minimal change disease (MCD) in 22 children (73%), mesangial proliferative glomerulonephritis in 6 children (20%), and focal segmental glomerulosclerosis (FSGS) in 2 children (7%). Four children in the asymptomatic group and all children in the NS group were administered prednisolone and/or cyclosporine. Normal urinalysis results were found in 8 children in the asymptomatic group and 3 children in the NS group during the follow-up period of 3 to 15 years. Eight children in the NS group were frequent relapsers at the latest follow-up. Two children with FSGS (1 child, asymptomatic group; 1 child, NS group) received dialysis 10 and 15 years after the diagnosis. There were no differences in histological findings and clinical outcomes between the 2 groups. Four children with MCD in the NS group underwent a second biopsy. C1q deposits disappeared in 2 children, and 1 of these 2 children showed FSGS. CONCLUSION: Childhood C1q nephropathy is found in a wide clinical spectrum. Some children showed disappearance of C1q deposits through the follow-up period. A large number of children with C1q nephropathy showed MCD. However, FSGS may develop in some children on repeated biopsy. Therefore, long-term follow-up is needed in children with C1q nephropathy.

Adolescent↗
PubMed1982

Three step purification of C1q by DNA precipitation, ion exchange and lectin affinity chromatography.

The difficulties associated with the isolation of pure C1q in sufficient amounts are reflected by the substantial number of isolation procedures, which are being published. The two major problems are a low yield and contaminating immunoglobulins. In addition, some isolation protocols appear to produce C1q contaminated with an inhibitor (C1q-INH). The present isolation protocol involves precipitation of C1q by DNA, chromatography using Sephadex QAE A 50 followed by Con A affinity chromatography. By this combination of purification steps maximal advantage was taken of the cationic properties and high carbohydrate content of the C1q molecule. The yield was 1-2 mg C1q per 100 ml serum. The isolated C1q was free of any demonstrable contaminants as demonstrated by Ouchterlony double diffusion and polyacrylamide gel electrophoresis.

Chromatography, Affinity↗
PubMed1990

[Clinical significance of the level of circulating immune complexes in patients with small cell bronchial carcinoma].

In the sera of 58 bronchial cancer patients with different TNM progression stage the relative 125I-C1q binding activities (BA) were determined before, after an induction of polychemotherapy and after a simultaneous polychemo- plus X-rays therapy. Only a statistically non-significant decrease of the 125I-C1q-BA was measured in the sera of patient groups with a stronger metastatic spread in the regional lymph nodes or distant metastasis. The tumor therapy cycles changed the serum 125I-C1q-BA differently and non significantly. The determination of serum 125I-C1q-BA of bronchial cancer patients is not relevant clinically.

Antigen-Antibody Complex↗
PubMed1988

The development of a C1q anti-C1q immunoadsorbent for removal of immune complexes from plasma.

An immunoadsorbent based on immobilized C1q has been developed to remove possibly pathogenic immune complexes from plasma deriving from patients suffering from systemic lupus erythematosus or rheumatoid arthritis. Traditional immobilization procedures based on, e.g., cyanogen bromide activation could not be used to produce an efficient adsorbent. However, by using antibodies directed towards C1q as handles for the immobilization of C1q it was possible to make an adsorbent that efficiently bound immune complexes in plasma. The capacity of the C1q anti-C1q adsorbent to bind artificial immune complexes such as aggregated human globulins or immune complexes from various plasma samples was evaluated. Both batch and column experiments were conducted. The typical capacity in batch was about 1 mg immune complexes/ml gel when incubated with patient plasma samples with high titers of immune complexes. Special attention has to be paid to leakage of undesirable components from the adsorbent. It was found that leakage of C1q occurred but it was not more than after covalent immobilization procedures such as cyanogen bromide.

Antigen-Antibody Complex↗
PubMed1982

Immune complexes in progressive systemic sclerosis (scleroderma).

Serum immune complexes were measured in 92 patients with progressive systemic sclerosis, and elevated levels were found as follows: Raji cell assay 72% (59% after pronase treatment of Raji cell), agarose gel electrophoresis 52%, and C1q binding 24%. Forty-three (47%) had abnormal results on two or more of these tests, but only 17 (18%) had normal results by all three assays. Computer-assisted analysis of immune complex results and extensive clinical and laboratory data compiled on these patients revealed that the patients with abnormal Raji cell assays more often had diffuse scleroderma, tendon friction rubs, and positive serum antinuclear antibody tests than did patients with negative results on Raji cell assays. Individuals with immune complexes detected by C1q binding had evidence of pulmonary involvement and positive serum rheumatoid factor more frequently than did patients whose C1q tests were negative.

Adolescent↗
PubMed1988

An ELISA technique for the measurement of C1q in cerebrospinal fluid.

Determination of the C1q content of cerebrospinal fluid (CSF) may be of value in understanding the immunological reactions occurring within the central nervous system (CNS). A double sandwich ELISA method has been developed for the detection of C1q in human serum and CSF. It uses polyclonal antibodies and is sensitive in the nanogram range. The mean concentrations of C1q were determined to be 127 micrograms/ml in serum and 0.4 microgram/ml in CSF. These results suggest that increased levels of C1q in the CSF play a role in some neurodegenerative disorders.

Adolescent↗
PubMed1992

IgG subclass restriction of autoantibody to solid-phase C1q in membranoproliferative and lupus glomerulonephritis.

The IgG subclass distribution for autoantibodies to solid-phase C1q (anti-spC1q) in sera from 14 patients with membranoproliferative glomerulonephritis (MPGN) and 10 patients with systemic lupus erythematosus (SLE) nephritis was determined by an enzyme-linked immunosorbant assay employing C1q as the immunosorbant in the presence of 2 M NaCl to prevent Fc binding and monoclonal anti-human IgG subclass reagents. The autoantibody to spC1q in MPGN, especially in types I (7 patients) and II (3 patients), was almost entirely restricted to IgG3. In contrast, in SLE anti-spC1q was completely restricted to IgG2 in 3 patients while predominantly IgG2 in the other 7 patients. The different subclass restriction of anti-spC1q in these two disorders suggests that antibody formation is either in response to different epitopes on the collagen-like region of C1q or that patients with SLE and MPGN mount different immunologic responses to the same antigenic stimulus.

Analysis of Variance↗
PubMed1982

The use of TNP-conjugated polyacrylamide beads in a C1q binding inhibition test for circulating immune complexes.

A new assay for the detection of circulating immune complexes is described. It is based on the same principle as the C1q deviation test: the binding of radiolabelled C1q to a solid phase is inhibited by immune complexes. Trinitrophenylated polyacrylamide beads are used as a stable C1q-reactive solid phase in our test. Aggregated IgG in normal serum could be detected by this method to a minimum concentration of about 10 microgram/ml. The test was used to quantitate circulating immune complexes in sera of patients with glomerulonephritis, liver diseases, lymphoma, and myeloid leukemia. The results are compared and correlated with those obtained by the C1q binding assay for the same sera.

Acrylic Resins↗
PubMed1987

The immunosuppressive activity of C1q degradation peptides.

We have previously reported the existence and activity of a collagen-like, low molecular weight, suppressive peptide complex in patients with greater than 40% BSA burns. Since C1q participates in the inflammatory response and contains a collagen-like sequence, we have tested, in vitro, the putative generation and immunologic activity of C1q peptide fragments under physical conditions present in burned patients. Nanogram quantities of heat- and enzyme-generated fragments of C1q were shown to be suppressive in vitro to neutrophil chemotaxis, and the mixed lymphocyte response (MLR). The addition of lymphocytes pretreated with C1q fragments suppressed ongoing MLR, indicating the activation of suppressor cells by the peptides. Rabbit anti-C1q globulin was found to reduce the suppressive activity of the collagen-like suppressor which was isolated from human burn sera. Our results therefore suggest that C1q may be an early source of degradation peptides which have strong nonspecific immunosuppressive activity following thermal injuries.

Burns↗
PubMed2003

Diagnostic and prognostic significance of anti-C1q antibodies in systemic lupus erythematosus.

PURPOSE OF REVIEW: The presence of a wide variety of autoantibodies is a characteristic finding in systemic lupus erythematosus. Autoantibodies against nuclear proteins, such as anti-nuclear and anti-double-stranded DNA antibodies, are used as diagnostic markers in systemic lupus erythematosus. Renal involvement is frequently found in systemic lupus erythematosus and is an important risk factor for death. Therefore, markers for the diagnosis and follow-up of nephritis are very important. Anti-C1q autoantibodies are strongly associated with renal involvement in systemic lupus erythematosus. This study will review recent findings on the pathogenic role and clinical importance of anti-C1q antibodies in lupus nephritis. RECENT FINDINGS: Recent clinical studies have clearly emphasized the diagnostic relevance of anti-C1q autoantibody levels in patients with lupus nephritis. With a possible negative predictive value of 100%, anti-C1q autoantibodies are the only exclusive antibodies associated with the involvement of a single organ in systemic lupus erythematosus. Next to the clinical findings, the pathogenic significance of anti-C1q antibodies has been shown in an animal model. The deposition of autologous C1q in healthy glomeruli of mice after the infusion of anti-C1q antibodies induces moderate tissue damage. SUMMARY: The latest insight into the pathogenesis of anti-C1q autoantibodies in the development of lupus nephritis and the recently demonstrated clinical importance of anti-C1q autoantibodies for the diagnosis of lupus nephritis support the value of further investigations. New diagnostic methods for the detection of anti-C1q and an accurate follow-up of antibody levels might be of use in clinical practice.

Autoantibodies↗
PubMed1988

C1q enhances the phagocytosis of Cryptococcus neoformans blastospores by human monocytes.

We investigated whether C1q, a subunit of the first component of C, could modulate human peripheral blood monocyte-mediated phagocytosis of Cryptococcus neoformans (CN). Adherence of monocytes to C1q-coated surfaces induced a significant enhancement of ingestion of CN blastospores that had been opsonized with specific anticapsular IgG (IgG-CN). Additionally, C1q enhanced the monocyte-mediated phagocytosis of CN opsonized with C (CN-absorbed, nonimmune, normal human serum; C-CN). Ingestion of IgG- and C-CN by control and C1q-stimulated monocytes was maximal by 1 h of incubation. The monocyte-mediated enhancement of phagocytosis caused by C1q was paralleled by a proportionate increase in fungicidal activity, an effect which was maximal by 3 h of incubation. Human serum albumin-adherent, control monocytes exhibited only a low level of killing after 3 h of incubation. C1q enhancement was blocked by preincubation of the surfaces with a goat, polyclonal F(ab')2 anti-C1q. This study describes a new cellular function for the cell surface C1q receptor: the enhancement of phagocytosis of a pathogenic organism by monocytes.

Adjuvants, Immunologic↗
PubMed1984

Critical aspects of the 125I-C1q binding assay for detecting immune complexes in tumor patients.

Clinical studies on C1q binding activity in tumor patients showed contradictory results and it was suggested that methodical problems might be partly responsible for those discrepancies. Therefore, precision of the C1q binding assay when testing tumor sera, influences of assay modifications on test results and possible interfering substances were investigated. Compared to aggregated human IgG and BSA: anti-BSA complexes as standards the C1q binding material in tumor sera was more unstable after freezing-thawing and distinctly more susceptible to methodical influences like testing with different 125I-C1q preparations or variations of PEG concentration and ionic strength of PEG solution. Addition of heparin and fibrinogen influenced the C1q binding of some tumor sera more than the C1q binding of standards and normal sera. Thus, instability and sensitivity to methodical influences of the C1q binding material have to be considered, when clinical studies using the C1q binding assay to detect immune complexes in tumor sera are interpreted.

Antigen-Antibody Complex↗
PubMed1993

Complete functional C1q deficiency associated with systemic lupus erythematosus (SLE).

A complete functional deficiency of C1q is described in a patient suffering from SLE. From reduced plasma C1 activity of the parents a hereditary trait was assumed. The defective C1q molecule was haemolytically inactive, did not bind to immune complexes, and was not recognized by the monocyte C1q receptor. C1 activity in the patient's serum could be restored by the addition of purified C1q. Analysis by gel-filtration and ultracentrifugation experiments revealed an immunoreactive molecule of about 150 kD mol. wt, corresponding to one structural subunit of the C1q macromolecule, containing two A chain-B chain dimers and a C-C chain dimer. Applying Southern blot analysis with cDNA clones encoding for the three individual chains of the C1q molecule, no restriction fragment length polymorphism was detected, ruling out possible major alterations of the genetic information.

Adult↗