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PubMed1996

Autoantibodies to the collagen-like region of C1q are strongly associated with classical pathway-mediated hypocomplementemia in systemic lupus erythematosus.

We have investigated the presence of autoantibodies to the collagen-like region (CLR) of C1q and its relationship with classical pathway-dependent hypocomplementemia in patients with SLE. Antibodies to CLR/C1q were quantitated in the plasma of 113 unselected patients with SLE by ELISA, using purified CLR as antigen. Plasma concentration of C3, CH50 activity and C2 hemolytic activity were determined according to standard procedures. The prevalence of IgG antibodies to CLR/C1q in the study population was 33.6%. Plasma titers of anti-CLR/C1q autoantibodies showed a strong negative correlation with CH50 activity (p < 0.0001) and with plasma levels of C3 (p < 0.0001). Eighty-five percent of patients with severe complement consumption exhibited high titers of anti-CLR/C1q antibodies in plasma, independently of clinical disease activity. Anti-CLR/C1q antibodies were present in the plasma of 38% of patients with moderate classical pathway consumption and 14% of patients with no evidence of complement consumption. Analysis of sequential samples from six patients over a period of 18 to 24 months demonstrated that changes in CH50 activity mirrored those of the plasma titers of anti-CLR/C1q antibodies. Acquired hypocomplementemia through the classical pathway is strongly associated with the presence of anti-CLR/C1q autoantibodies in SLE. The results suggest that anti-CLR/C1q antibodies may perpetuate classical pathway activation, independently of clinical disease activity.

Autoantibodies↗
PubMed1981

Age influences the clinical and serologic expression of systemic lupus erythematosus.

The clinical and serologic characteristics of 17 patients with onset of systemic lupus erythematosus (SLE) after age 50 were compared with those of 49 younger patients. All patients were followed prospectively for a mean duration of 47 months. A clinical and serological data base was established for each patient, and information collected at each visit to a lupus clinic was analyzed by computer. The clinical featured distinguishing old-age SLE were a low incidence of significant renal disease and prominent pleuropericarditis and arthritis throughout the period of followup. Serologic abnormalities were milder in older patients. Thus, hypocomplementemia, anti-DNA antibodies, and C1q precipitins occurred less frequently, and rheumatoid factor was more often present than in younger patients with SLE. Regression analysis suggested linear change in disease expression with age rather than distinct age-related subgroups.

Adult↗
PubMed1994

Rhinosporidiosis: immunohistochemical and electron microscopic studies.

Sixteen biopsies of rhinosporidiosis (15 nasal and one conjunctival) from 16 Southern Indian male immigrant workers showed mucosal lymphoplasmacellular infiltrates together with transepithelial elimination of nodular bodies and destruction of some late stage nodular bodies in histiocytic granulomata with central neutrophilic microabscesses. Early nodular bodies were immunohistochemically positive for alpha 1-AT, alpha 1-ACT, CEA, S100, fibronectin, amyloid-p-component, IgG, IgA, C1q and C3. Electron microscopy showed organized concentric lamellated bodies in early nodular bodies and not in end-stage nodular bodies which contained mostly amorphous electron dense materials. Structures formerly regarded as 'sporangia' and 'spores' are believed to be lysosomal bodies loaded with indigestible residues to be cleared via transepithelial elimination or segregated/destroyed by secondary immune/granulomatous responses.

Adult↗
PubMed1983

Direct immunofluorescence in recurrent aphthous ulcers and Behçet's disease.

Direct immunofluorescence (IF) investigations in oral aphthae were performed in 17 patients with recurrent aphthous ulcers (RAU) and in 9 patients with Behçet's disease (BD). In addition, cutaneous hyperreactivity lesions from 2 BD patients were examined. The results were compared to direct IF findings in 28 patients with nonaphthous oral diseases. There was no difference between direct IF on oral aphthae in RAU compared to BD. Deposition of C3 in vessel walls of the subepithelial connective tissue was observed in 13 of 17 patients with RAU and in all patients with BD. IgM deposits in vessel walls were found in 5 RAU and 3 BD patients. Deposition of C1q or C4 was not present. By contrast, IgG and/or IgM, C1q, C3 and C4 were detected in dermal vessel walls of skin hyperreactivity lesions from 2 BD patients. This finding is considered to be a true immune complex vasculitis. Compared to nonaphthous oral lesions, oral aphthae of BD and RAU were characterized by C3 deposition in the subepithelial vessel walls.

Adolescent↗
PubMed2005

Generation and characterization of a novel tetravalent anti-CD22 antibody with improved antitumor activity and pharmacokinetics.

The purpose of this study was to prepare a tetravalent anti-human CD22 recombinant antibody with improved antitumor activity and a half life longer than that of its divalent counterpart. We compared the ability of tetravalent vs. divalent antibody to associate/dissociate to/from CD22-positive Daudi cells, to interact with murine and human Fcgamma receptors (FcgammaR), to bind human complement component C1q, to inhibit the growth of tumor cells, to diffuse into various tissues, to be internalized by Daudi cells, to react with human neonatal Fc receptors (FcRn), and to persist in the circulation of normal mice. As compared to the murine or chimeric divalent antibodies, the chimeric tetravalent counterpart has a longer half life in mice. It also has an affinity for FcRns that is identical to that of human IgG. The tetravalent antibody has increased antitumor activity in vitro and completely conserved effector functions (binding to FcgammaR-positive cells and to C1q) in vitro. Despite its 33% higher molecular weight, it penetrates mouse tissues as well as its divalent antibody counterpart. Based on the improved in vitro performance and pharmacokinetics of the tetravalent antibody it will now be tested for its antitumor activity in vivo.

Animals↗
PubMed2003

Severe pulmonary hypertension associated with primary Sjögren's syndrome.

Severe pulmonary hypertension is one of the fetal complications in various connective tissue diseases. We report a case of severe pulmonary hypertension associated with primary Sjögren's syndrome. In a lung biopsy specimen, there were findings of intimal and medial hypertrophy with narrowing vessel lumina and plexiform lesions. Moreover, deposits of immunoglobulin M, immunoglobulin A and complement protein C1q were found in the pulmonary arterial walls. Although pulmonary hypertension was refractory to oral prostacyclin, steroid therapy improved the clinical and hemodynamic conditions. In the present case, the immunological etiology may be related to the mechanisms of pulmonary hypertension associated with Sjögren's syndrome.

Adult↗
PubMed1981

Serum and blister fluid immune complexes in bullous pemphigoid: detection with C1q and monoclonal rheumatoid factor.

Eighty serum samples and 24 blister fluids from 51 patients with active bullous pemphigoid were tested for the presence of immune complexes by both a monoclonal rheumatoid factor (mRF) inhibition radioassay and a C1q-binding radioassay. Forty-two of the 80 serum samples were positive by the mRF assay, while 27 were positive by the C1q-binding assay. Antibody titres to the basement membrane zone did not correlate with levels of circulating immune complexes. Thirteen of 24 blister fluids had detectable immune complexes by the C1q assay, while only seven of 24 blister fluids were positive by the mRF assay. Sucrose density-gradient ultracentrifugation studies suggest that the mRF- and C1q-reactive substances in both bullous pemphigoid sera and blister fluids are of a size compatible with immune complexes. Although immune complexes are detectable in a high percentage of bullous pemphigoid patients, their role in this disease may be epiphenomenal rather than pathogenetic, merely reflecting the presence of autoantibody and soluble antigen.

Antigen-Antibody Complex↗
PubMed1985

Characterization of C1q, C1s and C-1 Inh synthesized by stimulated human monocytes in vitro.

C1q, C1s and C1 Inh synthesized and secreted by human monocytes were characterized by SDS-PAGE. C1q is formed of three chains A (Mr approximately 35 000), B (Mr approximately 33 000) and C (Mr approximately 25 000) which are associated in two subunits A-B and C-C. It appears identical to C1q purified from plasma. C1s is secreted as a non-activated, monocatenar protein of Mr approximately 87 000 identical to proenzymic C1s from plasma. Secreted C1 Inh (Mr approximately 100 000) has a slightly higher Mr than purified plasmatic C1 Inh. Monensin treatment of the cells favours the intracytoplasmic accumulation of products at various glycosylation stages.

Cells, Cultured↗
PubMed2005

Glycosaminoglycans inhibit neurodegenerative effects of serum amyloid P component in vitro.

Serum amyloid P component, a member of pentraxin serum protein family, has been suggested to contribute to the progression of neurodegeneration including Alzheimer's disease by binding to beta-amyloid fibrils leading to an increased stability of the deposits against proteolytic degradation and by inducing neuronal apoptosis. Here, we show that glycosaminoglycans inhibit both the serum amyloid P component-beta-amyloid interaction and the neurotoxic effect of serum amyloid P component. These effects correlate with the structure of glycosaminoglycans and show different structure-activity relationship in the case of the two different effects. While the efficacy of the inhibition on the serum amyloid P component-induced cell death increases with the uronic acid content, the inhibitory activity on the serum amyloid P component-beta-amyloid interaction decreases with the increasing uronic acid content of the glycosaminoglycans. The inhibitory effect of glycosaminoglycans on the interaction between the first component of the complement cascade (C1q) and beta-amyloid shows a similar structure-activity relationship as on the serum amyloid P component-beta-amyloid interaction. This suggests that glycosaminoglycans interfere with the binding site on beta-amyloid for serum amyloid P component and C1q. The functional consequence of this binding has been demonstrated by heparin which promotes the proteolysis of beta-amyloid in vitro in the presence of serum amyloid P component. Our results suggest that glycosaminoglycans might have therapeutical potential on the neurodegeneration reducing its progress.

Alzheimer Disease↗
PubMed2003

Characterisation and properties of ectosomes released by human polymorphonuclear neutrophils.

Human neutrophils release vesicles when activated in vitro and in vivo, in local and systemic inflammation. We have suggested that the presence of these vesicles is due to ectocytosis, defined as the release of rightside-out oriented vesicles expressing a select set of membrane proteins. Herein we have characterised the vesicles released by neutrophils to be ectosomes with specific properties. They contained cytosolic F-actin indicating their outside-out orientation. They bound Annexin V, suggesting that they expose phosphatidylserine, similarly to platelet microparticles. They expressed a subset of cell surface proteins (selectins and integrins, complement regulators, HLA-1, FcgammaRIII, and CD66b, but not CD14, FcgammaRII, and CD87). There was no specificity for transmembrane or glycosyl-phosphatidylinositol-linked proteins and, unexpectedly, L-selectin, known to be cleaved from the surface of activated neutrophils, was present. Ectosomes exposed active enzymes released by neutrophils upon degranulation (matrix metalloproteinase-9, myeloperoxidase, proteinase 3, and elastase). In particular, released myeloperoxidase was able to bind back to ectosomes. The purified complement protein C1q and C1q from serum bound to ectosomes as well. Another aspect of ectosomes was that they became specifically adherent to monocytic and endothelial cells. These observations suggest that neutrophil-derived ectosomes have unique characteristics that make them candidates for playing roles in inflammation and cell signaling.

Actins↗
PubMed2006

Further description of early clinically silent lupus nephritis.

Thirty silent lupus nephritis (SLN) patients were compared to 16 individuals bearing overt lupus nephritis (OLN). Results included: years of systemic lupus erythematosus (SLE) diagnosis were significantly earlier (4.6 +/- 2.8 years) in SLN than in OLN (7.18 +/- 3.61) (P < 0.05). Neurological compromise, hypertension, normocitic anemia and lymphopenia were significantly prevalent in OLN than in SLN (P < 0.05). Beside normal urinary sediment and renal function tests, the SLN group showed a moderate increase of both activity (AI) and chronicity (CI) renal pathology index when compared to highly increased AI and CI in OLN (P < 0.05). Seventy percent of SLN patients were ISN/RPS Classes I (6.6%) and II (63.3%) while 81% of OLN cases were Classes III, IV (37.5%) and V. IgG, IgA, IgM, lambda chain, C3 and fibrinogen immune deposits were found in 90% or over in both SLN and OLN individuals while in 60% or over, both groups also showed kappa chain, Clq and C4 deposits. While prevalence of ANA, anti-dsDNA and anti-C1q antibodies were similar in both groups, anti-histone, anti-RNP, CIC and CH50 serum levels were significantly different in OLN versus SLN (P < 0.05). We strongly suggest that indeed SLN is the earliest stage in the natural history of lupus nephritis.

Adult↗
PubMed1981

Association between circulating immune complexes and renal disease in New Zealand mice.

Using female NZB x NZW (B/W) F1 x NZW backcross mice, analyses were made to determine the correlations among C1q- binding and conglutinin (Kg) binding immune complexes in the circulation and the proteinuria of the B/W F1 mice. There was a significant association between the development of proteinuria and the high serum level of Kg-binding immune complexes, while no significant association was seen between the proteinuria and the C1q-binding immune complexes in the backcrosses. There was a lack of correlation between these C1q-binding and Kg-binding immune complexes. These results suggest that the major immune complexes detected by these two methods differ in nature and emphasize that the demonstration of antigen-non-specific immune complexes in the circulation do not necessarily mean that these immune complexes are responsible for the pathogenesis of the particular disease being studied.

Animals↗
PubMed1997

The effect of mannan-binding lectin on opsonophagocytosis of Neisseria meningitidis.

Mannan-binding lectin (MBL), an acute phase protein with a structure and a function very similar to that of C1q, is known to act as an opsonin binding to a number of microorganisms. In order to investigate the effect of MBL on the phagocytic killing of meningococci, a serogroup B meningococcal strain (H44/76) and its unencapsulated variant v24, as well as a serogroup A meningococcal strain were opsonized with MBL (purified from normal human plasma at the State Serum Institute, Denmark) and used in a phagocytic killing assay at a density of 7 x 10(3) CFU/ml. Polymorphonuclear cells (PMNs) from one healthy donor were isolated by density gradient centrifugation over Percoll and added to the system (7 x 10(6) cells/ml). In a first set of experiments without addition of serum or complement, no influence of MBL was observed on the killing of any of these strains. Addition of MBL to non-opsonized bacteria of the serogroup A strain did not result in enhanced killing either; on the contrary, the growth of this strain increased significantly when a high MBL concentration (40 micrograms/ml) was used in the presence of PMNs. Further investigations were performed using sera of five individuals with late complement component deficiency (LCCD) and a concomitant MBL deficiency, vaccinated with a tetra-valent (ACYW135) meningococcal capsular polysaccharide vaccine. Pre- and post-vaccination sera (50% final concentration) were tested against a group A strain opsonized or not with MBL. In only one patient was there a moderate increase of killing of the opsonized bacteria after vaccination compared to pre-vaccination serum. Our results suggest that MBL may not play a significant role in the opsonophagocytosis of meningococci, irrespective of its binding to unencapsulated and serogroup A strains.

Bacterial Vaccines↗
PubMed2003

Immunologically induced, complement-dependent up-regulation of the prion protein in the mouse spleen: follicular dendritic cells versus capsule and trabeculae.

The expression of the prion protein (PrP) in the follicular dendritic cell network of germinal centers in the spleen is critical for the splenic propagation of the causative agent of prion diseases. However, a physiological role of the prion protein in the periphery remains elusive. To investigate the role and function of PrP expression in the lymphoid system we treated naive mice i.v. with preformed immune complexes or vesicular stomatitis virus. Immunohistochemistry and Western blot analysis of the spleen revealed that 8 days after immunization, immune complexes and vesicular stomatitis virus had both induced a strong increase of PrP expression in the follicular dendritic cell network. Remarkably, this up-regulation did not occur in mice that lack an early factor of the complement cascade, C1q, a component which has been shown previously to facilitate early prion pathogenesis. In addition to the variable PrP level in the germinal centers, we detected steady and abundant PrP expression in the splenic capsule and trabeculae, which are structural elements that have not been associated before with PrP localization. The abundant trabeculo-capsular PrP expression was also evident in spleens of Rag-1-deficient mice, which have been shown before to be incapable of prion expansion. We conclude that trabeculocapsular PrP is not sufficient for splenic prion propagation. Furthermore, our observations may provide important clues for a physiological function of the prion protein and allow a new view on the role of complement and PrP in peripheral prion pathogenesis.

3T3 Cells↗
PubMed1983

Sural nerve immune deposits in polyneuropathy as a remote effect of malignancy.

Sural nerves from six patients with polyneuropathy as a remote accompaniment of malignancy were studied by light microscopy, immunofluorescence, electron microscopy, and immuno-electron microscopy. Sural nerves also were studied in twelve control patients with malignant diseases without peripheral neuropathy and in fifteen with neuropathy associated with nonmalignant conditions. Only nerves from the first group of six patients showed immune deposits of immunoglobulin M, C3, and C1q as granular or confluent layers in the inner laminae of the perineurium as well as in and around endoneural capillaries. The findings are similar to those in published studies of Waldenström's macroglobulinemia, chronic relapsing polyneuropathy, and neuropathy of monoclonal gammopathy and extend the list of conditions to include several forms of carcinoma and Hodgkin's disease.

Adult↗
PubMed1992

Circulating immune complexes in patients with psoriasis: do they exist?

Sera from 16 patients suffering from active psoriasis without arthropathy (2 guttate, 10 nummular, and 4 mixed type) were examined for the presence of circulating immune complexes. Five routine laboratory assay systems were used, based on C1q-binding or detection of IgG-coupled C1q and C3-breakdown products. In 14 patients, no elevated levels of circulating immune complexes were detected. One patient, who additionally suffered from late-phase HIV-1 infection, showed C1q-binding activities as well as levels of IgG-coupled C1q and C3-breakdown products in four of the assay systems, which indicated the presence of immune complexes in his serum. In another patient, with nummular psoriasis, slightly elevated levels of circulating immune complexes were measured by two of the assay systems. These results question the hypothesis of an essential pathogenic role of circulating immune complexes in psoriasis.

Adult↗
PubMed1984

Murine lupus nephritis: effects of cyclophosphamide on circulating and tissue bound immunoreactants.

We investigated the effects of cyclophosphamide (Cy) on immunoreactants of plasma and kidney of mice with lupus nephritis. Cy therapy decreased plasma concentrations of IgG, but not the concentrations of anti-DNA antibodies, C3, and C1q reactive materials; in glomeruli deposits of immunoreactants were mesangial in location and decreased overall. Although Cy arrested the nephritis of NZB/W mice, the anti-DNA activity in the renal eluates was very low and comparable in untreated and in treated mice. Immune complex systems other than, or in addition to, DNA-anti-DNA are likely to play a role in the pathogenesis and course of murine lupus nephritis.

Animals↗
PubMed1981

Circulating immune complexes in human acute leukaemia.

Circulating immune complexes (CIC) in the sera of 60 newly diagnosed leukaemic patients were investigated by two methods, 125I-C1q binding test (C1q-BA) and conglutinin binding assay (KgB-SP). Positivity percentages were respectively 20.0% (C1q-BA) and 28.3% (KgB-SP). The small overlap between the results of the two methods suggests the occurrence of different types of CIC. The presence of CIC was found to be related only to clinical haemorrhage and thrombocytopenia; it did not prove to affect the prognosis and the survival of leukaemic patient.

Acute Disease↗