Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement Inactivator Proteins”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1983

C3 nephritic factor and hypocomplementaemia in a clinically healthy individual.

Nephritic factor was detected in an individual whose serum showed a selective decrease in the third component of complement (C3) during and subsequent to an illness resembling disseminated gonococcal infection (DGI). As is characteristic of C3 nephritic factor (C3NeF), its activity was heat stable, was associated with IgG, and enhanced cleavage of normal human serum C3 via the alternative pathway. However, unlike previously reported cases of C3NeF detection in association with glomerulonephritis and/or lipodystrophy, this patient has had no significant disease before or more than 2 years after the apparent DGI. The significance of C3NeF in a healthy individual is unexplained, but this study suggests its occurrence may be more ubiquitous than previously suspected.

Adult↗
PubMed1980

Human seminal plasma inhibition of complement.

Recent studies have shown that human seminal plasma contains chemically and biologically distinct factors which inhibit lymphocyte functions and the serum bactericidal and opsonic activities associated with the killing of gram-negative organisms. Because of the direct association between complement action and serum bactericidal and opsonic activities, inhibition of complement may be one of the possible mechanisms of action of seminal plasma immunoinhibitory factors. Complement hemolytic activity was measured for C3 and C4 in serum Neisseria gonorrhoeae and Escherichia coli bactericidal reaction mixtures with and without addition of seminal plasma. In the presence of seminal plasma, where there was no bactericidal action, C3 and titers were reduced to approximately 50% of the titers in the reactions with complement donor serum. The C3 titers were lower than in the reaction mixtures with immune serum and complement donor serum, where N. gonorrhoeae bactericidal activity occurred. Individual human seminal plasma specimens depressed CH50 activity of pooled normal human sera up to 50% of normal levels. There were no differences in inhibition by seminal plasma specimens from normal or vasectomized men. Treatment with seminal plasma depressed the functional activity of complement components C1 and C3 by more than 50%. Seminal plasma also inhibited alternate pathway activity. Cleavage of factor B was demonstrated. The seminal plasma factor which inhibited complement was of low molecular weight. DPF blocked the seminal plasma complement-inhibitory factor. However, amidolytic activity for serine protease substrates could not be demonstrated. It is likely that the seminal plasma complement inhibitor is a protease inhibitor acting singly or in combination.

Absorption↗
PubMedDate not supplied

Inhibition of complement by gold sodium thiomalate.

The effect of gold sodium thiomalate on C3 and factor B activation by monosodium urate monohydrate (MSUM) and zymosan was studied using a quantitative immunoelectrophoretic assay for complement activation. C3 and factor B conversion by the classical pathway activator MSUM, was inhibited 50% and 100% by 3.2 x 10(-4)M and 10(-3)M gold sodium thiomalate, respectively. C3 and factor B conversion by the alternative pathway activator, zymosan, was much less susceptible to inhibition by gold. Gold at 10(-3)M, inhibited alternative pathway activation by only 30%. A 50% inhibition would have required 10(-2)M gold. There was no significant inhibition of complement activation through either pathway by less than 10(-4)M gold. Sodium thiomalate alone showed no inhibition. Studies using other crystals and immune complexes were confirmatory. Thus, there was no appreciable inhibition of the complement system at concentrations of gold attainable in the serum of patients receiving chrysotherapy. The in vivo significance of these findings is unknown.

Complement C3↗
PubMed1981

Partial characterization of a Trypanosoma cruzi-released decomplementing factor.

Trypanosoma cruzi releases a factor (SCAF) when grown in vitro which decomplements normal mouse, human, and guinea pig sera. The production and potency of SCAF was dependent on the density of cultured parasites, parasite viability and proliferative capacity, and duration of culture. The in vitro interaction between SCAF and serum complement (C') occurred rapidly and was complete within 30 min of mixing. The administration of SCAF to normal mice resulted in up to 50% reduction in hemolytic C' activity, whereas SCAF had no effect on the C' levels in mice infected wit T. cruzi for more than 10 days. The active moiety of SCAF was shown to be a nonproteinaceous substance(s) with a molecular weight of approximately 23,000 daltons.

Animals↗
PubMed1983

[Complement consumption as criterion of the tolerogenicity of a globulin preparation].

Experiments on mice (296 animals) were made to study the capability of native and deaggregated preparations of human globulin to fix complement as well as the relationship of this indicator to tolerogenic properties of the preparations in question. Ultracentrifuged preparations were discovered to have the decreased capability to activate complement. As anticomplementary properties of the preparations become more demonstrable their tolerogenicity declines. The decreased capability to activate complement can be used as criterion in screening tolerogenic preparations.

Animals↗
PubMed1983

Meningococcal meningitis associated with persistent hypocomplementaemia due to circulating C3 nephritic factor.

Two teenage patients who presented with meningococcal meningitis were found to have persistently low C3 levels even after recovery. This was accompanied by circulating C3 nephritic factor, which persisted for more than 12 months in each case. Neither patient had evidence of partial lipodystrophy or of glomerulonephritis initially, although one patient subsequently developed mesangioproliferative glomerulonephritis following a second admission with pneumococcal pneumonia. It is possible that the generation of the nephritic factor was initiated during the presenting illness.

Adolescent↗
PubMed1981

[Mechanisms of action and clinical importance of C3-nephritic-factor (author's transl)].

The C3-nephritic-factor is an autoantibody specific against C3-convertases. This IgG-immunoglobulin is particularly found in patients suffering from membranoproliferative glomerulonephritis and causes a complement-activation under elimination of physiological regulator mechanisms. The clinical importance of this factor is discussed.

Complement C3 Nephritic Factor↗
PubMed1980

Herpes gestationis associated with the C3 nephritic factor.

Herpes gestationis (HG) is a rare, blistering disease of pregnancy and the puerperium that has immunologic findings of C3 with or without IgG deposited in a linear, band-like distribution along the dermoepidermal basement membrane zone (BMZ). A circulating IgG factor has been demonstrated that will fix complement by the classic pathway in vitro. This study involves a patient who had classic HG with C3 at the BMZ, and who had a circulating factor with activity via the alternative complement pathway similar to the previously described C3 nephritic factor found in patients with partial lipodystrophy, systemic lupus erythematosus, and membranoproliferative glomerulonephritis. Like the C3 nephritic factor, the activity was detected in IgG fractions of serum samples.

Adult↗
PubMed1980

Variation in the susceptibility of bovine mycoplasmas to killing by the alternative complement pathway in bovine serum.

All but one of nine Acholeplasma strains were susceptible to killing by gnotobiotic-calf serum while all but one of fifteen Mycoplasma strains were resistant. The mechanism of killing was examined using inhibitors of complement, viz. EDTA. MgEGTA. epsilon-amino caproic acid, and also by desalting serum and adding MgCl2 and CaCl2. The results indicated that, when strains were killed by serum from gnotobiotic calves it was by the alternative complement pathway. However, experiments with mycoplasmas and Escherichia coli indicated that the effect of MgEGTA was not identical for bovine and human sera. Sensitivity to killing by the alternative complement pathway in bovine serum appeared to be a property of avirulent strains and resistance to killing may be regarded as a virulence determinant of mycoplasmas.

Acholeplasma↗
PubMed1981

Complement activation in nonsystemic glomerular diseases in children.

All forms of glomerulonephritis (GN) in man seem to be immunologically mediated and the complement system appears as one of the most important mediators of renal injury. The study of complement activation is therefore of great help in the identification of the immunopathogenic process involved in the various types of glomerular diseases. After a review of the molecular events of complement activation and the methods used to study the complement system in man, we will attempt to summarize current knowledge concerning complement in nonsystemic glomerular diseases frequently encountered in children. The terms used are those descriptive of glomerular morphology as defined either by light microscopy and electron microscopy (endocapillary-proliferative GN with humps, extramembranous GN, membranoproliferative GN) or by immunofluorescent microscopy (mesangial IgA GN).

Basement Membrane↗