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PubMed1976

Immunoglobulin and complement deposition in skin of rheumatoid arthritis and systemic lupus erythematosus patients.

Rheumatoid arthritis (RA) was differentiated from systemic lupus erythematosus (SLE) by direct immunofluorescent techniques on skin specimens, using monospecific antisera for IgG, IgM, C3, C1q, properdin, and fibrin. Of 30 patients with RA studied, 20 had dermal vessel deposits of immunoglobulins and complement components in unaffected skin without the characteristic dermal-epidermal junctional fluorescence of SLE. Of 24 SLE patients studied, 24 had granular deposits of immunoglobulins and complement components in unaffected skin at the dermal-epidermal junction.

Arthritis, Rheumatoid↗
PubMed1980

Immunochemical quantitation of complement components of Clq and C3 in sera and synovial fluids of patients with bone and joint diseases.

The amount of the initiating complement component (Clq) in the classical pathway and the first essential component (C3) in the alternative complement pathway were measured with a single radial immunodiffusion (SRID). A high ionic strength was used corresponding to that of 0 . 25 M NaCl and 0 . 01 M EDTA to avoid nonspecific binding of Clq with immune aggregates. Measurements were made on sera and/or synovial fluids from 165 patients with various bone and joint diseases. Values of Clq and C3 in synovial fluids were also expressed as ratios to that of albumin in the same specimens to avoid the influence of differences in volume of synovial fluid in various diseases, and this appeared to provide a reliable index reflecting pathological conditions. Both serum Clq and C3 levels were raised highly in rheumatoid arthritis, gout, and osteomyelitis, but the extent of the elevation of C3 was less conspicuous. Values of Clq and C3 in synovial fluids also markedly increased in rheumatoid arthritis.

Adolescent↗
PubMed1980

Failure to find C1q-binding material and anti-IgG antibodies in ankylosing spondylitis.

C1q-binding immune complexes (C1C), anti-IgG antibodies (anti-IgG Ab), and complement levels were investigated in the serum of 37 patients with ankylosing spondylitis (AS). In all these studies the mean levels observed in patients with AS were similar to those in 31 normal subjects. Moreover, no significative difference in either CIC or anti-IgG Ab levels was observed when the patients were classified in different clinical forms according to the localisation (peripheral and central) or to the gravity (mild and severe) of the AS. In a parallel study increased CIC and anti-IgG Ab levels were found in most of the 81 patients with seropositive or seronegative rheumatoid arthritis.

Antibodies, Anti-Idiotypic↗
PubMed1988

Complement mediated inhibition of immune precipitation in rheumatoid arthritis: studies on interaction of heat aggregated IgG with IgM rheumatoid factor.

Serum samples from patients with seropositive rheumatoid arthritis contain an inhibitor of complement mediated inhibition of immune precipitation (CMIP). This inhibitory effect can be produced by the addition of either purified monoclonal or polyclonal IgM rheumatoid factor (RF) to human serum. The specificity of the rheumatoid factor influences the degree of inhibition, and when precipitation occurs the rheumatoid factor coprecipitates with the antigen-antibody complex. In rheumatoid sera there was a significant positive correlation between IgM RF concentration and inhibitory activity, though the range of inhibitory activity seen for the same concentration of rheumatoid factor was considerable. Small quantities of heat aggregated IgG (HAGG) had a much greater effect on the measurement in an enzyme linked immunosorbent assay (ELISA) of IgM RF than they did on the inhibitory activity of IgM RF in the CMIP assay. Larger quantities of HAGG initiated complement activation and increased the precipitation of immune complexes. IgM RF reduced the complement activating properties of HAGG by reducing the amount of Clq which bound to the aggregate. The mechanisms by which IgM RF overcomes CMIP in rheumatoid sera may involve its inhibitory effects on the binding of Cl to the antigen-antibody complex.

Antigen-Antibody Complex↗
PubMed1976

Complement and meningococcal infection.

Serum C3 levels were measured in 211 patients with meningococcal disease. Low levels were found in 13 patients with acute meningococcaemia, and complement activation may have contributed to the peripheral circulatory collapse that was responsible for nine deaths. The complement profile of these patients suggested activation of both classical and alternative complement pathways. Patients with meningitis had a higher mean serum C3 level than controls. Serial studies in 13 serum antigen-positive patients with meningitis who subsequently developed arthritis or cutaneous vasculitis showed a transient fall in serum C3 in eight. This fall was probably due to the formation of immune complexes that were responsible for their allergic complications.

Adult↗
PubMed1976

Immunological studies in pre-eclamptic toxaemia.

Although five patients with severe pre-eclamptic toxaemia (PET) had increased anticomplementary activity in their serum, there was no evidence of complement activation in the plasma of four of the five patients. These results are not implicated in the pathogenesis of PET. No significant correlation was found between anticomplementary activity and pregnancy-associated alpha2-glycoprotein.

Antigen-Antibody Complex↗
PubMed1977

Humoral immune system in inflammatory bowel disease: I. Complement levels.

Serum levels of complement components Clq, C4, C3, and Properdin factor B, from the classical and alternative pathways of complement activation, have been estimated in patients with ulcerative colitis and Crohn's disease. C3, factor B, and to some extent C4 concentrations all increased when the disease was active. In remission the levels of these components did not differ from hospital control patients. There was no evidence for the preferential consumption of the proteins of either pathway of activation, even in those patients with evidence of circulating immune complexes.

Colitis, Ulcerative↗
PubMed1980

Increased C1q binding and arthritis in primary biliary cirrhosis.

Using the C1q binding assay, circulating immune complexes were detected in 31 of 50 (62%) patients with primary biliary cirrhosis and 17 of these had arthritis. This took the form of a seropositive inflammatory polyarthritis in 12 of 18 patients with C1q binding greater than or equal to 20%, whereas a milder seronegative arthritis associated with scleroderma and Raynaud's phenomenon was found in five of 13 patients with C1q binding < 20%. Only two of the 19 patients with normal binding had arthritis and this was of a mild and transient nature. There was a positive correlation between C1q binding and the serum concentrations of IgG and IgM. Results also supported the hypothesis that circulating immune complexes may be involved in the development of arthritis in patients with primary biliary cirrhosis.

Aged↗
PubMed1981

Prevalence and persistence of C1q binding activity in healthy subjects.

Samples of serum from 885 normal healthy blood donors were tested for the presence of soluble immune complex-like material by a solid-phase C1q binding assay. The majority of donors (93%) had low or undetectable levels of C1q binding activity in their sera, but 6% had levels that were clearly outside the normal distribution. When these individuals were retested after several weeks half of them still had elevated levels of C1q binding activity.

Antigen-Antibody Complex↗
PubMed1989

Circulating immune complexes after splenectomy.

Circulating immune complexes were evaluated in 25 patients (age range 10 to 46 years) who had undergone splenectomy for non-malignant conditions by studying a polyethylene glycol insoluble serum fraction. Although the extent of binding to Clq was within normal limits, these patients had increased concentrations of factor B in the immune complex serum fraction. These findings indicate that an unusual type of circulating immune complex may be detected after splenectomy, suggesting a possible role for the spleen in the removal of circulating immune complexes.

Adolescent↗
PubMed1975

Complement.

Explore the source record for details and available documents.

Anaphylaxis↗
PubMed1975

The autinglobulin test in autoimmune hemolytic anemia.

The foregoing summarizes what can be learned from a carefully performed antiglobulin test using specific antisera. Clinical syndromes can be more easily considered, and mechanisms of destruction can be more certainly discerned.

Anemia, Hemolytic, Autoimmune↗
PubMed1986

Inherited complement component abnormalities.

Inherited deficiencies of early complement components are frequently associated with immune/rheumatic disorders and recurrent (Neisserial) infection with deficiency of late complement components. The genetic complexity of complement components is further demonstrated by electrophoretic allotypy and analysis of DNA restriction fragment length polymorphisms.

Adult↗
PubMed1976

Role of complement components on cells and in cell interactions.

The complement system, though complex, is relatively easy to study both in terms of its reaction pathways, its distribution and its genetics. There is reason to believe that the complement system is involved in cell surface events and interactions at a variety of levels and we may hope that the knowledge of the system in the blood plasma will provide relatively easy insights into the more difficult areas with cells.

Antigen-Antibody Reactions↗
PubMed1979

Immune deposit nephritis and single-component cryoglobulinemia associated with chronic lymphocytic leukemia. Evidence for a role of circulating IgG-anti-IgG immune complexes in the pathogenesis of the renal lesion.

2 patients developed the nephrotic syndrome several years after diagnoses of chronic lymphocytic leukemia. In both cases light microscopy showed membranoproliferative glomerulonephritis. Electron microscopy and immunofluorescent staining revealed electron-dense deposits and deposition of immunoglobulins and C3. Both patients had single-component IgG cryoglobulinemia. The eluted glomerular-bound protein contained IgG only. IgG in patients' sera, cryoglobulins, and kidney eluate had kappa light chains only. Immune complexes were detected in the sera and in the cryoglobulins by the Clq binding test. Immunoadsorption studies revealed anti-IgG antibodies in the patients' sera, cryoglobulin, and kidney eluate. Direct immunofluorescent studies using the patients' sera, cryoglobulins, and kidney eluate on frozen sections of patients' kidneys were positive, providing additional evidence for the immune complex nature of the glomerulonephritis. The immunohistochemical studies of our patients are suggestive of the presence of circulating IgG-anti-IgG immune complexes and their possible involvement in the pathogenesis of the glomerulonephritis and the nephrotic syndrome in these 2 cases.

Antigen-Antibody Complex↗
PubMed1981

Activation of the alternative complement pathway by unidentified substances in human glomerulonephritis.

Activation of the alternative complement pathway (AP) has been investigated in 79 serial serum samples obtained from 28 patients which had different types of glomerulonephritis. Serum factors activating the AP of the complement system have been detected in 12 patients with various forms of glomerulonephritis. Immune complexes (IC), levels of complement components of the classical and the alternative pathways and cobra venom factor activity were measured. Serum specimens were subcategorized as 2 study populations: (i) patients with serum factors activating AP and (ii) patients with both serum activators and IC. Although CoVF-AH50, properdin factor B and C3 concentrations were comparably depressed in these two groups, the levels of Clq and C4 were very low only in patients with circulating IC. These data were highly suggestive of AP activation due to serum factor. In contrast the patients also showing circulating IC had activation of both pathways. The presence of these factors suggests that renal damage can be determined by other immunological stimuli.

Antigen-Antibody Complex↗