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PubMed2000

Characterization of the murine homolog of C1qR(P): identical cellular expression pattern, chromosomal location and functional activity of the human and murine C1qR(P).

Human C1qR(P) is a highly glycosylated transmembrane protein that is the human C1q receptor/receptor component that in vitro mediates enhancement of Fc- and C3b-mediated phagocytosis. A human genomic clone and a murine genomic clone that is 73% identical in sequence with the coding region for human C1qR(P) cDNA have been isolated. Chromosomal localization of the human and murine gene demonstrates that these genes are syntenic. Murine cell lines of diverse myeloid origins are shown to respond to interaction of C1q with the enhancement of phagocytosis similar to that seen previously in human peripheral blood monocytes. Northern blot, RT-PCR, Western blot and FACS analyses demonstrated that mC1qR(P) is expressed in these murine myeloid cell lines, but not in a mouse epithelial cell line, similar to the cell type expression of the human gene product. A polyclonal antibody to a peptide sequence common to the deduced sequence from the both murine and human C1qR(P) inhibited the enhancement of phagocytosis response to C1q when cells were permeabilized to permit access of the antibody to the intracellular milieu. These data support the postulate that the identified murine and human genes are homologs, confirm the previously predicted intracellular location of the C-terminus of the molecule, and indicates the necessary role of this intracellular domain in transducing the signal that leads to enhancement of phagocytic function.

Amino Acid Sequence↗
PubMed1995

Anti-collagen antibodies and immune complexes in equine joint diseases.

An investigation was made into the possible contribution of autoimmune mechanisms to equine arthropathies. Serum and synovial fluid (SF) immune complexes and anti-collagen Type II antibodies were measured, by ELISA, in groups of horses with naturally occurring osteoarthritis (OA), osteochondritis dissecans (OCD), bone fracture, traumatised joints, synovitis, infected joints and non-diseased (control) joints. Significantly raised anti-collagen Type II antibodies were found in osteoarthritic (P < 0.02) and traumatised joint synovial fluids (P < 0.01) compared with the control, where ten of 38 (26%) OA and five of eight (63%) traumatised joint synovial fluid samples had raised anti-collagen Type II antibodies (above mean and 2 SD of control group; P < 0.05). Significantly raised levels of C1q-binding immune complexes were found in the synovial fluids of horses with OA (P < 0.001), OCD (P < 0.02), fractured articular bone (P < 0.001), infected (P < 0.01) and traumatised joints (P < 0.001) as compared with the control horses. Raised C1q-binding activity (above mean and 2 SD of control group; P < 0.05) was shown in synovial fluids in 18 of 38 (47%) OA, four of 16 (25%) OCD, four of nine (44%) fractured bone, one of eight (14%) synovitis, two of four (50%) infected joints and seven of eight (88%) traumatised joints. No raised anti-collagen Type II antibodies or C1q-binding activity were detected in sera from any clinical group. Correlations were found, in synovial fluids, between anti-collagen Type II antibodies and C1q-binding activity in OA (P < 0.02), synovitis (P < 0.01) and infected joint (P < 0.05) groups. Within individual horses, there were no correlations between the SF and sera measurements of either anti-collagen II or C1q-binding activity. The relationship between cause and effect of these immunological findings cannot be determined; as they are common to many types of equine joint disorder it is probable that they are not an initiating factor in pathology.

Animals↗
PubMed1983

A solid phase C1q enzyme assay for circulating immune complexes adapted for routine clinical laboratory testing.

An assay for circulating immune complexes (CIC) that is adaptable to a routine clinical laboratory is described. This solid phase C1q (SP C1q) enzyme immunoassay (EIA) uses commercially available reagents and is reproducible with CV% of less than 20% in the abnormal range. We also demonstrate the specificity of the assay for detecting clinically relevant dsDNA-anti-DNA immune complexes.

Antibodies, Anti-Idiotypic↗
PubMed1981

Correlation between circulating antigens detected by the radioimmunoprecipitation-polyethylene glycol assay (RIPEGA) and C1q-binding immune complexes in human schistosomiasis mansoni.

Circulating schistosome antigens (CSA) and circulating immune complexes (CIC) were investigated in serum from 420 patients infected with Schistosoma mansoni. The radioimmunoprecipitation-polyethylene glycol assay with [125I] anti-S. mansoni rabbit antibodies appeared as a sensitive and specific method to quantify CSA. In fact, more than 75% of the patients showed significant levels of CSA. C1q-binding CIC were also detected in 70% of subjects with schistosomiasis. In addition, a close correlation was observed between levels of CSA and CIC. These data suggest that part of the CIC present in human schistosomiasis are formed by schistosome specific antigens.

Antigen-Antibody Complex↗
PubMed1989

[Serum complement composition of myasthenia gravis].

Serum complements of C1q C1, C4, BF, C1-INH and C5 were measured by single immunodiffusion in 54 patients with myasthenia gravis (MG), 46 normal control (NC) and 42 cases of other neurological disorders. It was found that C1-INH, C5 levels in MG were significantly higher than that in other groups (P less than 0.01). The serum levels of C1-INH, C5 were not related to the clinical type and the stage of the illness. These data suggest that endplate receptors might be disrupted through complement mediated immunoreaction.

Adult↗
PubMed1990

Enhancing effect of C1q on IgG monoclonal antibody binding to hapten.

We have previously demonstrated that IgG antibody binding to microfilariae of Dirofilaria immitis increased in the presence of purified C1q. The present study was designed to examine the mechanism of the C1q effect using a system with an antihapten monoclonal antibody (MoAb) and a hapten as an antigen. Microtiter plates were coated with 4-hydroxy-3-nitrophenyl-acetyl (NP)-bovine serum albumin (BSA), and mouse anti-NP MoAb (IgG) was added in the presence of C1q. The amount of IgG which bound to NP-BSA increased with the addition of C1q (p less than 0.01) when the antibody had both specificity to the antigen and ability to fix C1q. The C1q effect, examined using two anti-NP MoAbs with different affinities, was more apparent with the low-affinity antibody (LAMoAb) than with the high-affinity (HAMoAb; percent enhancement of IgG binding was 19 vs. 12%). The C1q effect on LAMoAb binding was doubled when a small amount of HAMoAb was incubated with LAMoAb. The C1q effect on IgG binding might be operative in the early phase of infection, where a small amount of high-affinity antibody and a relatively large amount of low-affinity antibody are produced in the host.

Adjuvants, Immunologic↗
PubMed2005

Anti-C1q autoantibodies in lupus nephritis: prevalence and clinical significance.

Recently, anti-C1q autoantibodies have been proposed as a useful marker in systemic lupus erythematosus (SLE) since their occurrence correlates with renal involvement and, possibly, with nephritic activity. We aimed to evaluate the prevalence of anti-C1q antibodies in patients with SLE, with and without renal involvement, and to correlate these markers' presence and levels with the activity of the disease and nephropathy. We studied 61 patients with SLE, 40 of whom had biopsy-proven lupus nephritis; 35 patients with other connective tissue diseases; and 54 healthy controls. In addition, 18 lupus nephritis patients were followed up during the disease time course. Anti-C1q antibodies were measured using "homemade" ELISA with high salt concentration (1 M sodium chloride). High anti-C1q antibody titers (> 55 AU) were present in 27 of 61 (44%) SLE patients and in 4% and 0% of normal blood donors and pathologic controls, respectively. Anti-C1q antibodies were found in 60% of patients with lupus nephritis compared with only 14% of SLE patients without nephropathy (P < 0.05). Moreover, patients who were positive for anti-C1q antibodies had a higher European Consensus Lupus Activity Measurement (ECLAM) score (4.35 vs. 2.2); 89% of patients with active lupus nephritis showed high titers of anti-C1q antibodies compared with 0% of patients with inactive nephritis. Anti-C1q and anti-dsDNA antibodies agreed in 79% of cases. Our results confirm that anti-C1q antibodies are present in a significant percentage of SLE patients, and that their presence and levels correlate with disease activity-in particular, during renal flare-ups.

Antibodies, Anti-Idiotypic↗
PubMed1999

Epidermal nuclear CIq deposits in a patient with amyopathic dermatomyositis.

We report a case of amyopathic dermatomyositis, in which C1q deposits on the epidermal nucleus were immunohistologically found as well as Ig deposits at the dermoepidermal junction (DEJ). Direct immunofluorescence (IF) examination of infiltrated erythematous lesions revealed C1q deposits on the epidermal nucleus and fibrinogen at the DEJ, and examination of hyperkeratotic erythematous lesions showed linear deposits of Ig G and Ig A at the DEJ but not in the nuclei of epidermal cells. The authors discuss the direct in vivo interaction between nucleus and immunoreactants in dermatomyositis.

Aged↗
PubMed1988

Anticardiolipin antibodies in systemic sclerosis: immunological and clinical associations.

Anticardiolipin antibodies of IgG/IgM class were detected in seven of 28 patients with systemic sclerosis including five of 16 patients severely affected by extensive visceral disease. This severely affected sub-group also showed significant elevations of plasma levels of von Willebrand factor antigen in 10 cases and serum C1q binding activity in seven cases respectively. This triple association raises the possibility that multiple immunological mechanisms are involved in the pathogenesis of systemic sclerosis and its vascular lesions.

Adult↗
PubMed2006

Protruding disordered loop of gC1qR is specifically exposed and related to antiapoptotic property in germ cell lineage.

We established a monoclonal antibody (MAb), 5G9, with the use of a fixed seminoma tissue from an archival paraffin-embedded specimen, as an immunogen. Without antigen retrieval, positive 5G9-immunohistochemical staining was confined mostly to primordial germ cells, spermatogonia and various germ cell tumors. 5G9 recognized a mitochondrial 32-kD protein with an isoelectric point of pH 4.2, identified as a multifunctional ubiquitous protein, receptor for globular head of C1q (gC1qR), whose epitope was mapped in a disordered loop connecting the beta3 and the beta4 strands. Reflecting the ubiquitous distribution of gC1qR, with antigen retrieval, 5G9 was found reactive to a wide range of normal and tumor tissues. Since several co-precipitated and phosphorylated bands were observed in various human cell lines but not in germ cell tumor cell lines by in vitro phosphorylation assay, we speculate that the epitope of gC1qR is specifically unmasked in the germ cell lineage. By reducing gC1qR by siRNA, a significant increase was observed in the number of apoptotic cells in ITO-II and TCam-2 cell lines, but to a lesser extent in the Colo201 colon cancer cell line, showing an antiapoptotic property of gC1qR in the germ cells. Since protein-protein interaction is partially preserved by fixation, archival paraffin-embedded specimens can be a valuable source of immunogens for generating monoclonal antibodies (MAbs) that recognize tissue-specific protein conformation.

Antibodies, Monoclonal↗
PubMed2002

Herpes simplex virus type 1 evades the effects of antibody and complement in vivo.

Herpes simplex virus type 1 (HSV-1) encodes a complement-interacting glycoprotein, gC, and an immunoglobulin G (IgG) Fc binding glycoprotein, gE, that mediate immune evasion by affecting multiple aspects of innate and acquired immunity, including interfering with complement components C1q, C3, C5, and properdin and blocking antibody-dependent cellular cytotoxicity. Previous studies evaluated the individual contributions of gC and gE to immune evasion. Experiments in a murine model that examines the combined effects of gC and gE immune evasion on pathogenesis are now reported. Virulence of wild-type HSV-1 is compared with mutant viruses defective in gC-mediated C3 binding, gE-mediated IgG Fc binding, or both immune evasion activities. Eliminating both activities greatly increased susceptibility of HSV-1 to antibody and complement neutralization in vitro and markedly reduced virulence in vivo as measured by disease scores, virus titers, and mortality. Studies with C3 knockout mice indicated that other activities attributed to these glycoproteins, such as gC-mediated virus attachment to heparan sulfate or gE-mediated cell-to-cell spread, do not account for the reduced virulence of mutant viruses. The results support the importance of gC and gE immune evasion in vivo and suggest potential new targets for prevention and treatment of HSV disease.

Animals↗
PubMed1996

The C1q binding activity of IgG is modified in vitro by reactive oxygen species: implications for rheumatoid arthritis.

IgG can be denatured in vitro by reactive oxygen species (ROS). Native IgG activates the complement cascade through C1q. Using a modified ELISA, C1q binding activity of rheumatoid IgG has been compared to IgG denatured by neutrophil-derived ROS. The C1q binding activity of rheumatoid synovial fluid IgG is greater than the corresponding serum IgG (P < 0.01). Denaturation of IgG by activated polymorphs or the Fenton reaction decreased its C1q binding activity (P < 0.01). In vitro exposure of IgG to OH. and ROO. increased its interaction with C1q (P < 0.01). Hypochlorous acid had no effect. ROS-induced alteration to IgG-C1q binding activity may promote the inflammatory response in rheumatoid arthritis.

Adult↗
PubMed1984

Immune complexes in juvenile chronic arthritis.

Twenty children with juvenile chronic arthritis (JCA) and two children with SLE were investigated as to the existence of immune complexes in a long-term survey over 24 months. Two different methods were applied, a solid phase C1q RIA and a polyethylene glycol precipitation test. Detection of immune complexes was compared to the course of the disease and other laboratory data. C1q RIA showed a distinctly higher number of positive tests than the PEG precipitation test. The presence of immune complexes appears to be transitory in the course of JCA, as was demonstrated by C1q RIA. A connection with a more advanced stage of the disease is postulated. The positive test can be regarded as a prognostic parameter which, however, cannot be used for the diagnosis of JCA.

Adolescent↗
PubMed1995

Circulating immune complexes in chronic hepatitis C.

For assessing the role of circulating immune complexes (CIC) in chronic hepatitis C, the relative frequency of CIC was determined in 54 patients with chronic hepatitis C, 15 asymptomatic hepatitis C virus (HCV) carriers, and 54 healthy controls. IgM and IgG containing CIC were studied using both C1q and conglutinin (K) in an immunoglobulin-specific solid-phase enzyme immunoassay. CIC were a common feature of chronic hepatitis C with 96.3% of patients with at least one abnormal test result. The prevalence of elevated IgG-K, IgM-K, IgG-C1q, and IgM-C1q CIC was 70.3%, 50.0%, 64.8%, and 35.1%, respectively. The prevalence of IgG class CIC was higher than IgM class CIC (P = 0.038 for K-CIC and P = 0.01 for C1q-CIC, respectively). There is correlation between IgG-K CIC and IgG-C1q CIC (r = 0.445, P = 0.002), IgG-K CIC and IgM-C1q CIC (r = 0.348, P = 0.020), IgM-K CIC and aspartic aminotransferase (r = 0.321, P = 0.015), IgM-K CIC and alanine aminotransferase (r = 0.301, P = 0.027). Compared to patients with chronic persistent hepatitis and chronic lobular hepatitis, patients with chronic active hepatitis have a higher prevalence of elevated IgG-K CIC (77.2% vs. 40.0%, P = 0.029) and IgM-K CIC (56.8% vs. 20.0%, P = 0.038). The concentration of IgG-K, IgM-K, and IgM-C1q CIC in the former was significantly higher than that in the latter, respectively. In conclusion, IgG class CIC is the major type of CIC in chronic hepatitis C.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Pelvic inflammatory disease isolates of Neisseria gonorrhoeae are distinguished by C1q-dependent virulence for newborn rats and by the sac-4 region.

The virulence mechanism of Neisseria gonorrhoeae in pelvic inflammatory disease (PID) is not well understood, and an objective diagnostic method to identify patients with PID is lacking. We investigated the hypothesis that development of PID was associated with a C1q-dependent virulence property of gonococcal strains. Recent development of a C1q-dependent experimental model of gonococcal infection (S. Nowicki, M. Martens, and B. Nowicki, Infect. Immun. 63:4790-4794, 1995) created an opportunity to evaluate this hypothesis in vivo. Therefore, the virulence of 32 clinical isolates (18 PID isolates and 14 local infection [LI] isolates) was evaluated in experimental rat pups. A serum bactericidal assay was used to characterize a gonococcal serum-resistant (ser(r)) phenotype. PCR primers designed to amplify a suitable-size gonococcal sac-4 DNA fragment (unique for serum-resistant donor JC1) were used to evaluate the association of serum-resistant genotype sac-4 with two phenotypes: C1q-dependent virulence expressed in vivo and resistance to bactericidal activity of human serum expressed in vitro. Strains were also characterized by auxotyping and serotyping. Of 32 gonococcal strains, 15 (46.7%) caused C1q-dependent bacteremia in rat pups and were sac-4 positive and ser(r). However, of the 15 isolates, 13 (87%) represented strains associated with human PID and 2 (13%) were associated with LI. None of the strains that were completely serum-sensitive (ser(s)) and sac-4 negative produced C1q-dependent bacteremia in rat pups, suggesting that both ser(r) and sac-4 were required for infection. The serum-resistant recombinant recipient of sac-4 produced C1q-dependent bacteremia in the rat model similarly to the serum-resistant donor of sac-4; the serum-sensitive parent strain did not produce bacteremia. These data suggest that sac-4-mediated serum resistance conferred C1q-dependent virulence and is a unique characteristic associated with PID. These newly identified features may contribute to the understanding of the pathogenic mechanism of PID-associated strains and open perspectives for establishing novel diagnostic methods.

Animals↗
PubMed1993

Serum bactericidal activity and induction of chemiluminescence of polymorphonuclear leukocytes: complement activation pathway requirements in defense against Neisseria meningitidis.

Serum bactericidal activity and chemiluminescence (CL) responses of polymorphonuclear leukocytes (PMNL) to pathogenic Neisseria meningitidis serogroups B and W-135 and to nonpathogenic serogroup 29E were examined with pooled normal human serum depleted of the complement proteins C1q, factor D, properdin and C5. Purified C1q, factor D, properdin and C5 were added alone or in combination. For investigation of serogroup W-135 meningococci, a C1q, factor D and properdin-depleted postvaccination serum with high concentrations of anticapsular antibodies was also used. Serogroup B and W-135 cultured to log phase were resistant to the bactericidal activity of pooled normal human serum but were efficiently killed through the classical pathway alone when the bacteria were cultured to stationary phase. Nonpathogenic serogroup 29E meningococci in log or stationary growth phases were efficiently killed in serum, predominantly through the classical pathway. Serogroup W-135 meningococci grown to log phase were resistant to classical pathway-mediated bactericidal activity in postvaccination serum but were killed on addition of alternative pathway proteins. Stationary phase serogroup W-135 meningococci were killed through both pathways in the postvaccination serum. In the pooled normal human serum CL responses of PMNL were consistently more pronounced with fully reconstituted C1q, factor D, properdin, C5-depleted serum than with serum reconstituted with C1q, factor D and properdin suggesting contribution of actions related to terminal components. In the absence of C1q, serogroup W-135 meningococci in postvaccination serum induced a significant but delayed alternative pathway-mediated CL response. CL responses induced by serum-opsonized meningococci, in contrast to serum bactericidal activity, were not influenced by culture conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Bactericidal Activity↗
PubMed1984

A re-examination of the incidence of circulating immune complexes in normal pregnancy.

Circulating immune complexes were detected in 20% of serum samples from pregnant patients by the liquid-phase C1q-binding assay. Two other immune complex assays yielded negative results with the same samples. A careful case study was also carried out in which serum samples from before, during and after a normal pregnancy were analysed. The results are discussed in relation to the contradictory data previously published in this field.

Antigen-Antibody Complex↗
PubMed1990

Binding of C1q and DNA to support materials by means of a new coupling procedure.

Since several years matrix-bound biologically active substances are widely used in biosciences, biotechnology and medicine. We are presenting a simple and inexpensive activation procedure for support materials which allows stable binding of C1q and DNA. We could not found a remarkable leakage of the bound ligands. In connection with the good biocompatibility of our procedure, both are important for the application in extracorporeal immunoadsorption. The method is technologically simple and represents an alternative to the activation methods applied so far.

Biocompatible Materials↗