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[Circulating immune complexes in primo-secondary and serological syphilis (author's transl)].

Some clinical features of syphilis suggest that immune complexes may be a pathogenetic factor in the syphilitic lesions. Recently, circulating immune complexes have been reported in six patients with secondary syphilis by Søling et al. In our study, the presence of circulating immune complexes was investigated in 42 patients with syphilis (primary, secondary, serological) by the method of C1q binding test. Elevated C1q binding activity was demonstrated in two-thirds of the patients with primo-secondary syphilis, with a significant difference between this group and the controls. Only two of the 21 patients with serological syphilis showed elevated C1q binding activity. Circulating immune complexes, often at moderates rates, appear very early and decrease rapidly during treatment. It was not possible to demonstrate a decline in serum complement in association with elevated C1q binding activity. During five Jarisch-Herxheimer reactions, no increase in circulating immune complexes has been noticed compared to pre-treatment values: this suggests that circulating immune complexes have no essential importance in this reaction. The characterization of the components of these circulating immune complexes by the previously described "radioimmunoprecipitation PEG assay" (RIPEGA) will enable us to state their specificity and to conceive their potential responsibility in some lesions of secondary syphilis, such as nephrotic syndrome.

Adult↗

[Cryoglobulins and circulating immune complexes in rheumatoid arthritis. Clinical and biological correlations].

We studied circulating immune complexes using a test involving the precipitation of these complexes with polyethylene glycol 6000 at 2.5 percent, and characterization of the Clq bound in vivo to immunoglobulins in the serum of 126 healthy subjects, 95 hospitalized controls and 181 patients suffering from rheumatoid arthritis (RP). Likewise, the RP benefited from a study of cryoglobulins (CG). The PEG-Clq proved positive (PEG +) in 7 per cent of the healthy controls, 25 per cent in the seronegative RP. ThePEG & RP have a level of proteins, gammaglobulins, IgM and IgG that is higher than in patients in whom the test is negative. On the other hand, they have a lower level of C4. One CG was detected in 43 patients who were all PEG +. The level of CG is proportionate to the intensity of the articular inflammation, the sedimentation rate, the level of seric iron and that of hemoglobin. The composition of the precipitins obtained by activity of the PEG is very close to that of the CG.

Adolescent↗

[Serum levels of alpha-2-macroglobulin, ceruloplasmin, transferrin, alpha-1-antitrypsin and complement (beta-1-C) before and following 3- and 6-day injections of D-penicillamine in man].

UNLABELLED: The serum levels of alpha-1-antitrypsin, ceruloplasmin, transferrin, alpha-2-macroglobulin and complement (beta-1-C) were measured by the radioimmunodiffusion method of Mancini before treatment, after three days treatment with D-penicillamine (1,00 g. i. v. daily) and after treatment for 3 days with 2 x 1,00 g i. v. D-Penicillamine. The levels of alpha-2-macroglobulin, coeruloplasmin and transferrin dropped significantly after 3 days' treatment. Doubling the dosage for 3 days induced a further drop in transferrin and ceruloplasmin. The alpha-2-macroglobulin was not further influenced. The levels of alpha-1-antitrypsin and complement were not influenced by D-Penicillamine treatment. KEYWORDS: D-penicillamine, alpha-1-Antitrypsin, alpha-2-macroglobulin, transferrin, ceruloplasmin, complement (beta-1-C).

Adult↗

[Complement and nephritic activity in membranoproliferative glomerulonephritis].

A study of complement profiles and of "nephritic activity" (NeF activity) has been carried out in 33 children presenting with membranoproliferative glomerulonephritis (MPGN), in order to determine the pathway of complement activation. By morphological studies two varieties of MPGN have been distinguished. In MPGN with subendothelial deposits, immunofluorescent studies and complement profiles show an activation by the classical pathway. The demonstration of NeF activity in 7 of 20 patients suggests that there is recruitment of the amplification pathway. In MPGN with dense deposits, immunopathological studies indicate an activation of the complement system through the alternate pathway, NeF activity being present in 10 of 13 patients. With the functional tests used, it is not possible to ascertain that the factors responsible for the NeF activity in MPGN with subendothelial deposits are identical to the C3NeF identified in MPGN with dense deposits and/or partial lipodystrophy.

Capillaries↗

The activation of the C3b feedback cycle with human complement components. I. Through the classical pathway.

Reaction between the fourth, the oxidized second and the activated first components of human complement generated the stable enzyme C4oxy2 capable of cleaving the third component and depleting total complement in human serum. This enzyme was shown further to activate the C3b feedback cycle as shown by its ability to consume factor B in serum and the reduction in the extent of complement consumption in the presence of EDTA. OxyC2 on its own gave rise to C3 cleavage in normal human serum by a pathway needing classical pathway components. This unexpected finding suggests that there may be a 'C-1 tickover' in serum analogous to the 'C3b tickover'; the presence of oxyC2 allowing the 'capture' of the trivial amounts of C42 normally formed. In preliminary experiments in the rat, C4oxy2 was successfully formed in vivo, where it gave rise to cleavage of C3, consumption of C5, depletion of cobra venom factor cofactors and a biphasic change in the neutrophil count.

Animals↗

Complement-fixing islet-cell antibodies in type-I diabetes: possible monitors of active beta-cell damage.

Evidence is presented for the existence of a separate species of islet-cell antibodies which fix complement. Investigations in type I diabetics, non-diabetic polyendocrine patients, and unaffected first-degree relatives of type I diabetic probands show that the complement-fixing islet-cell antibodies are more closely related to the onset of clinical disease than the conventional islet-cell antibody, and they tend to disappear more rapidly. The complement-fixing antibodies may reflect damage of pancreatic beta cells more selectively and may be preferable to the conventional antibody as a serological marker for studying the natural history of type I diabetes.

Adolescent↗

Demonstration of circulating and tissue-fixed immune complexes in cutaneous necrotizing vasculitis.

Simultaneous demonstration of circulating and tissue-fixed immune complexes was attempted in 22 patients with cutaneous necrotizing vasculitis (7 anaphylactoid purpura, 9 cutaneous allergic vasculitis, 2 livedo reticularis, 1 thrombophlebitis, 2 erythema elevatum diutinum and 1 acute generalized pustular bacterid). In 16 out of the 22 patients, particularly patients with anaphylactoid purpura and cutaneous necrotizing vasculitis, there was a high Clq-binding activity. Decreased levels of C3 and C4 were seen in 2 and 3 patients, respectively. In 11 out of 16 skin lesions, the granular deposits of immunoglobulins and/or complement were demonstrated in the blood vessel walls of the dermis. IgA deposit was seen in anaphylactoid purpura, and IgM deposit in other types of vasculitis. C3 deposit was the most frequently noted. There was no definite correlation between Clq-binding activity and tissue deposits.

Antigen-Antibody Complex↗

In vitro inactivation of complement by a serum factor present in Junin-virus infected guinea-pigs.

A serum factor(s) of guinea-pigs infected with Junin virus, the etiological agent of Argentine haemorrhagic fever, is endowed with a potent anticomplementary activity. It is resistant to heat (56 degrees, 30 min) and elutes from a Sephadex G-200 column between albumin and haemoglobin. It is ineffective in the presence of EDTA or EGTA and does not sediment at 82,000 g. It has no direct effect on C4 unless functional Cl is present. However, it induces Cl activation that consumes C4 haemolytic activity in normal human and guinea-pig sera. The evidence presented in this report demonstrates that the complement activation observed in experimental Argentine haemorrhagic fever is at least in part due to a direct effect of this serum factor on the classical complement pathway.

Animals↗