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PubMed1977

Acute hepatitis: significance of changes in complement components.

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.

Acute Disease↗
PubMedDate not supplied

[Rapid method of measuring the alternative activity of the complement system].

The method is based on the ability of inulin to activate the alternative route of the complement system. The alternative activity is assessed from the consumption of the third complement component as a result of interaction with inulin. C3 is measured in experimental and control samples by kinetic titration, which permits assessing the activation of the alternative route in patients sera in less than 2 hours.

Complement C1↗
PubMedDate not supplied

[A method of preparing a reagent for assessing the activity of the second component and factor B of the complement system].

The method is intended for preparing a reagent for the detection of the second component and factor B of the complement system. It makes use of an unsophisticated device for even time-controlled heating of the serum by letting it pass through a coil pipe submerged in the bath. The resultant reagent is used to measure the activity of the second component and B factor of the complement system and may be used for assessing humoral immunity in patients.

Antibody Formation↗
PubMed1977

Relationship of levels of circulating immune complexes to histologic patterns of nephritis: a comparative study of membranous glomerulonephropathy and diffuse proliferative glomerulonephritis.

Immunofluorescent studies have suggested that immune complex deposition is the pathogenetic mechanism responsible for MGN and diffuse PGN. Despite this common mechanism, both renal disorders show considerable differences in the rate of progression of renal functional deterioration. To examine whether differences in the amounts of circulating immune complexes may in part be responsible for these differences, such complexes were assayed for in the sera of the two patient populations by a 1251-C1q binding assay, which has a lower limit of sensitivity for 75 microgram of aggregated human gamma globulin per milliliter of serum. Circulating complexes were found in sera from 11 of 14 patients with diffuse PGN but were undetectable in sera from 13 patients with MGN. Additional evidence for existing differences in the amounts of circulating immune complexes in the two groups was provided by serum C3 measurements. Serum C3 concentrations were below normal limits in nine of 14 sera from patients with diffuse PGN but were within normal limits for sera from all patients with MGN. Sucrose density gradient ultracentrifugation analysis of C1q reactive complexes showed them to have sedimentation coefficients ranging from 14.6S to 18.2S. The sizes of the complexes are consistent with those analyzed in animal models as being capable of inducing nephritis.

Antigen-Antibody Complex↗
PubMed1977

Immunologic evaluation of rheumatoid arthritis and therapy with levamisole.

The haemolytic complement activity and the complement components C3, C4 and C1q were significantly increased in the sera of 43 patients with classic or definite rheumatoid arthritis. The increased complement activity was fairly well correlated with an increased sedimentation rate, increased IgG levels and rheumatoid factor positivity. The E-rosette formation of T-lymphocytes measured in 16 rheumatoid arthritis patients was significantly depressed. These 16 patients were treated with levamisole 50 mg t.i.d. Four patients discontinued treatment because of side-effects. The remaining 12 patients were re-examined clinically and immunologically after a mean treatment period of 3.9 (range : 2.5-8) months. A significant reduction in haemolytic complement activity, C3, IgG and sedimentation rate and a significant increase in E-rosette forming cells were observed, and these were accompanied by a significant clinical improvement. These findings are discussed in view of the new concept that the basic defect in rheumatoid arthritis could be a disturbance of the interaction of T-and B-cells and faulty suppressor T-cells. According to this hypothesis, levamisole restores cell-mediated immune reactivity, thereby affecting the natural course of rheumatoid arthritis.

Adult↗
PubMed1977

Classical pathway complement activation in association with paraproteinaemia.

Five of twenty-three patients with paraproteinaemia (two IgM, three IgG) have been shown to exhibit marked classical pathway complement activation. The mechanisms of hypocomplementaemia proposed for the five patients are cryoglobulinaemia in one and in vivo immunoglobulin aggregation in the other four. Three further patients had a low C1q and three a low C3 unassociated with any other complement abnormality. No association with any particular IgG subclass or obvious clinical abnormality existed in association with hypocomplementaemia.

Complement C1↗
PubMed1977

Difference of anti-complementary effect of double stranded DNA and single stranded DNA.

Anti-complementary effect of both native double stranded DNA and denatured single stranded DNA was examined by the use of phage DNA of microgram level. The distinct difference of anti-complementary effect was detected between the double and single stranded DNA, that is, only single stranded DNA showed the anti-complementary effect. It is supposed that that the anti-complementary effect of single stranded DNA revealed by the present study is different from the anti-Clq effect which reported on both double and single stranded DNA by Agnello et al.

Complement C1↗
PubMedDate not supplied

[Partial lipodystrophy, hypocomplementemia and glomerulonephritis].

Renal involvement is found in 20 to 50% of cases of Partial lipodystrophy (PLD). We report 8 cases of PLD of which 6 had a glomerular nephropathy and 2 had no renal disease but all had persistent hypocomplementemia and 5 had circulating nephritic factor (C3NeF). The analysis of these cases and of all the cases reported in the literature shows the specificity of the glomerular involvement. Membranoproliferative glomerulonephritis (MPGN) with dense intramembranous deposits is a constant finding in PLD with renal involvement. This variety of MPGN is well known for being associated with persistent hypocomplementemia. However, the presence of hypocomplementemia and C3NeF in patients with PLD but without nephritis raises the question of the interrelationship between alternative pathway complement activation and the development of MPGN with or without lipodystrophy. There is no valid explanation in the present state of knowledge for the association of partial lipodystrophy hypocomplementemia, and MPGN. From the answer to this problem should emerge a better understanding of the role of complement in renal disease and in particular in the unusual form of glomerular injury seen in MPGN.

Adolescent↗
PubMed1976

The ultrastructure of C1t, a subcomponent of the first component of complement: an E.M. and ultracentrifuge study.

C1t is a 9.5 S alpha1 glycoprotein that has been shown to be a fourth subcomponent of the first component of complement. The m.w. of C1t was found to be 233,000 by sedimentation equilibrium in the ultracentrifuge. A subunit m.w. of 23,000 was obtained by sedimentation equilibrium in 5.95 M guanidinium chloride. No change in either m.w. was produced by prior reduction and alkylation. In the electron microscope characteristic pentagonal figures of 85 A diameter were observed together with rod-like figures which appear to be stacked assemblies of the pentagonal figures. These observations lead us to propose that C1t is a noncovalent, decameric protein with the subunits disposed at the vertices of two regular pentagons joined at one of their faces. A possible relationship between C1t and the P-component of amyloid is discussed.

Complement C1↗
PubMed1979

Circulating immune complexes in lupus erythematosus, scleroderma and dermatomyositis.

Circulating immune complexes (CIC) were measured by three different methods in serum from 17 patients with systemic lupus erythematosus (SLE), 3 patients with "hydralazine-induced" SLE-like syndromes, 14 patients with discoid lupus (DLE), 8 patients with systemic sclerosis and 5 patients with dermatomyositis. Immune complexes were detected in 13 of the 17 patients with SLE. All patients with lupus nephritis and typical exanthema had circulating immune complexes. The concentration of immune complexes was inversely correlated to serum complements C4 and C3. All 3 patients with "hydralazine-induced" SLE-like syndromes had circulating immune complexes that disappeared after withdrawal of the drug. Immune complexes were detected in 3 of the 14 patients with DLE; all 3 patients with CIC had wide-spread DLE. In systemic sclerosis, CIC were detected in only 1 of the 8 patients. Four of the 5 patients with dermatomyositis demonstrated CIC in serum. No complement consumption was detected in dermatomyositis and the immune complexes may have been secondary to tissue destruction.

Antigen-Antibody Complex↗
PubMed1976

Serum and glomerular complement in 205 cases of glomerulonephritis.

In 205 cases of GN the glomerular deposits of C3, C1q, C4, and C3A and the serum levels of the same complement components at the time of biopsy were studied. Alterations of serum complement profile were found only in acute GN, membranoproliferative GN and lupus nephritis, while glomerular deposition was observed with a different incidence and intensity in all nephropathies. A strict correlation between the intensity of deposits and the degree of hypocomplementaemia was found only in early acute GN and in active lupus nephritis.

Complement C1↗
PubMed1976

Routine assay for the detection of immune complexes of known immunoglobulin class using solid phase C1q.

A new, sensitive and quantitative technique for the routine estimation of immune complexes has been devised. The assay involved the binding of immune complexes to Clq linked to the surface of plastic tubes; the amount of immune complex bound is then determined by adding radiolabelled anti-human IgG. Immune complexes were detected in twelve out of thirty-one patients with systemic lupus erythematosus. The test should prove useful in the diagnosis of immune complex diseases and will be valuable in the evaluation of disease activity.

Antigen-Antibody Complex↗
PubMed1976

Measles infection. Involvement of the complement system.

The complement system was examined in fifty patients with acute, apparently uncomplicated measles; forty-six were children less than 10 years old. Twenty showed evidence of pathological complement activation. In thirteen of these the pattern was consistent with activation of the classical pathway while in the other seven data suggested utilization of an alternative pathway. An additional eleven patients had isolated reduction in Clq without alteration in concentration of other components; these were excluded from the classical pathway group. No patient had detectable immune complexes or C3 splitting activity in serum; however, it is suggested that the abnormal complement patterns observed are likely to indicate the presence of circulating immune complexes in a high percentage of patients with this infection.

Antigen-Antibody Complex↗
PubMed1998

Requirement for the alternative pathway as well as C4 and C2 in complement-dependent hemolysis via the lectin pathway.

Mannan-binding lectin (MBL) is a C1q-like molecule opsonic for several micro-organisms. MBL can activate C4, C2, and later acting complement components in the presence of serine proteases similar to but distinct from C1r and C1s via the lectin pathway of complement activation. We report here that mannan-coated MBL-sensitized erythrocytes are lysed via the lectin pathway in human serum-Mg-EGTA. The surprising occurrence of MBL-initiated lysis in the absence of calcium contrasts with the calcium requirement for C1q-initiated activation of C4 and C2. C2 is required, and lysis is significantly enhanced when indicator cells presensitized with C4 and then coated with mannan (EAC4-M) are used. The alternative pathway also is required, since lysis is lost when either factor D or factor B is removed and is restored upon reconstitution with the purified protein. Even though MBL is a C-type lectin, it is retained on mannan-coated erythrocytes in the absence of calcium. This contrasts with the absence of calcium-independent retention on mannan immobilized on polystyrene plates or beads, and helps explain the MBL-initiated hemolysis in Mg-EGTA. These investigations show that the alternative pathway as well as C4 and C2 of the classical pathway are required for complement-dependent hemolysis via the lectin pathway and provide a method for assay of lectin pathway-mediated complement activity in human serum that should be useful in unraveling the molecular interactions of this pathway.

Calcium↗
PubMed1998

A small molecular weight factor in aqueous humor acts on C1q to prevent antibody-dependent complement activation.

PURPOSE: Aqueous humor inhibits activation of the classic complement pathway; however, the mechanism of this inhibition is unknown. We have examined at the molecular level potential factors responsible for the inhibition, and we have tried to determine where in the complement pathway the inhibition takes place. METHODS: Fresh rabbit aqueous humor was size fractionated by centrifuge concentrators and by size exclusion column chromatography, and each fraction was assayed for inhibition of the classic complement pathway in a standard CH50 hemolytic assay. Fractions with inhibitory activity were assayed for protein and the presence of ascorbic acid and were subjected to heat treatment. To identify where in the pathway the inhibitor(s) function, the expression of activated complement components bound to the surface of antibody-coated erythrocytes was analyzed by flow cytometry using fluorescein isothiocyanate-labeled antibodies to specific complement components. In addition, hemolytic assays were performed for the function of individual complement components. RESULTS: The most potent inhibition of the classic pathway was in a fraction of aqueous humor of less than 1.3 kDa. The inhibitory activity in the fraction was unassociated with detectable protein or ascorbic acid, and it remained present after heat treatment. The functional analysis through flow cytometry and hemolytic assays for individual complement components showed that the inhibitor in the less than 1.3-kDa fraction caused a blockade in the complement pathway at the level of C1q. CONCLUSIONS: The aqueous humor contains a unique potent anticomplementary factor that has a molecular weight less than 1.3 kDa. This heat-stable inhibitory factor inhibits the classic pathway at the level of C1q. These results imply that within the eye the complement pathway is inhibited at the earliest steps of its initiation. Such inhibition would prevent production of complement products that mediate inflammation and chemotaxis of inflammatory cells. Therefore, as part of the adaptation of immune privilege, the ocular microenvironment is protected from inflammation induced by antigen-antibody complexes.

Animals↗