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PubMed1982

Biological significance of the C3 nephritic factor in membranoproliferative glomerulonephritis.

Serum levels of the C3 nephritic factor (C3NeF), an IgG autoantibody directed against the C3bBb convertase of the alternative complement pathway, and of eight complement components (C1q, C4, C3, C3d, C5, C9, fB and properdin) were measured in 109 serum samples from 27 patients with idiopathic membranoproliferative glomerulonephritis (MPGN) (type I, 20 cases, and type II, 7 cases) and 14 patients with secondary MPGN. Correlations between the concentrations of C3NeF, serum complement levels and progression of the renal damage were studied during the course of the disease in 14 patients with C3NeF activity. The results showed that (1) C3NeF activity was more frequent in patients with type II MPGN than in patients with type I disease; nevertheless there was a high incidence of this splitting activity in patients with secondary MPGN, (2) high levels of the complement components were present in patients with MPGN, (3) low levels of C3 occurred frequently in type II disease and in secondary MPGN, (4) there was no correlation between C3, fB and C3NeF levels, (5) the presence of C3NeF was associated with a more rapid deterioration of renal function. Longitudinal studies showed that serum levels of C3NeF were not satisfactory for monitoring the clinical course of the illness and, in this respect, are similar to the levels of other autoantibodies in patients with autoimmune disease. As MPGN is a clinical syndrome with various pathogeneses, we suggest that the autoantibody, C3NeF, should be considered only as a marker of some forms of MPGN.

Autoantibodies↗
PubMed1981

[Studies of complement, nephritic factor, and circulating immune complexes in chronic mesangiocapillary glomerulonephritis types I and II (author's transl)].

The complement components CH50, C3, C4, and C1q, factor B, nephritic factor (NF), and circulating immune complexes (CIC) have been studied in 22 patients with chronic mesangiocapillary glomerulonephritis (CMCGN). Of the 22 patients studied, eight had normal complement levels and 14 had hypocomplementemia with marked reductions of C3 and CH50. Of the latter 14 patients, nine disclosed an activation pattern that followed the alternate pathway, while in the other five the classical pathway was followed. The patients with hypocomplementemia following the alternate pathway and with positive NF activity (five cases) had a histologic pattern of type II CMCGN with dense deposits within the basal membrane, while those with hypocomplementemia following the classical pathway and negative NF activity disclosed a histologic pattern of type I CMCGN. The etiopathogenesis of these two types of glomerulonephritis remains to be elucidated. Although the presence of CIC is discussed and they are only rarely detected with the usual techniques, immune complexes have been implicated as possible responsible factors in these diseases. It has been demonstrated that the NF is an IgG with the characteristics of an autoantibody specific against the C3bB and C3bBb convertases of the alternate pathway, thus forming the trimolecular complex C3bBbNF. Because serum NF is frequently associated to type II CMCGN, it could be speculated that this trimolecular complex behaves as an immune complex, the convertase C3b beeing the antigen and the NF, the antibody, and that, under certain circumstances and because of its low molecular weight, it could cause nephritis by its deposit in the glomerular basal membrane.

Antigen-Antibody Complex↗
PubMed1981

Complement-inhibiting and anti-inflammatory properties of chlorazole fast pink 2BL.

Chlorazole fast pink 2BL inhibited the classical complement pathway in rat serum both in vivo and in vitro. The in vitro potency of chlorazole fast pink against the alternative pathway could not be assessed accurately but it was clearly less than that against the classical pathway. The compound appears to bind strongly to albumin with a resulting decrease in potency in undiluted as compared to diluted serum. Anti-inflammatory activity was observed in models of inflammation known to be highly complement-dependent (direct passive Arthus, zymosan oedema) but not in models in which complement is not involved (dextran oedema) or plays a minor role (carrageenan oedema).

Animals↗
PubMed1980

Effect of complement depletion on the induction of amebic liver abscess in the hamster.

Complement depletion in the hamster by cobra venom factor (CoF) gives a higher frequency and severity of lesions after intrahepatic inoculation of Entamoeba histolytica. The CoF-treatment does not alter the humoral immune response to amebae, indicating that its effect on the amebic liver abscess is not due to suppression of the immune response but rather to its effect on complement levels at the time of the protozoal infection.

Animals↗
PubMed1993

The possible role of membrane complement regulators in vasculitis.

Potentially, damage to endothelial cells of small vessel walls may be induced by the deposition of immune complexes and subsequent complement activation. The degree of deposition of C3b onto the endothelial cell surface under normal conditions is regulated by a number of membrane-bound regulators. Under inflammatory conditions various cytokines could potentially deregulate the expression and function of the membrane-bound complement inhibitors. Such a process could potentially increase the susceptibility of the endothelial cell layer to complement-mediated attack and provoke a vascular lesion.

Animals↗
PubMed1994

Complement-inhibiting activities of human CD59 and analogues from rat, sheep, and pig are not homologously restricted.

Human erythrocyte CD59 and analogues isolated from erythrocytes of rat, sheep, and pig were examined for their ability to protect erythrocytes from various species against lysis by C from homologous and heterologous sources. In all cases, incorporation of human CD59 or analogues from rat, sheep, and pig efficiently protected guinea pig erythrocytes against lysis by C homologous with the CD59. However, each of the CD59 analogues also conferred on guinea pig erythrocytes protection against C from most heterologous species. These results demonstrate that none of the CD59 analogues tested were species specific in their C-inhibiting activity. Erythrocytes from species other than guinea pig could not be protected by incorporation of any of the available CD59 analogues despite similar incorporation in all erythrocytes tested. We suggest that the presence of endogenous inhibitors on these other erythrocytes masks the activity of incorporated CD59. Evidence that is supportive of this hypothesis was provided by demonstrating that blocking the endogenous CD59 with mAbs rendered erythrocytes susceptible to inhibition by high dosages of incorporated CD59.

Animals↗
PubMed1994

Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium.

Activation of the complement (C) system has been documented in both experimental and clinical studies of myocardial infarction, but the exact time course and mechanisms leading to C activation have remained unclear. Our earlier postmortem study on human beings showed that formation of the membrane attack complex (MAC) of C was associated with loss of CD59 (protectin), an important sarcolemmal regulator of MAC, from the infarcted area. The recent discovery of a rat analogue of CD59 has now allowed the first experimental evaluation of the temporal and spatial relationship between C component deposition and loss of CD59 in acute myocardial infarction (AMI). After ligating the left coronary artery in rats the earliest sign of C activation, focal deposition of C3, was observed at 2 hours. Deposition of the early (C1, C3) and late pathway (C8, C9) components in the AMI lesions occurred at 3 hours. Glycophosphoinositol-anchored rat CD59 was expressed in the sarcolemmal membranes of normal cardiomyocytes. In Western blot analysis extracts of normal rat heart CD59 appeared as a band of 21 kd of molecular weight under nonreducing conditions. Loss of CD59 in the AMI lesions was observed in association with deposits of MAC from day one onward. Our results show that C activation universally accompanies AMI in vivo. It is initiated within 2 hours after coronary artery obstruction via deposition of C3, which may be due to generation of the alternative pathway C3 convertase in the ischemic area. Deposition of C1 and late C components also starts during the early hours (2 to 4 hours) after ischemia. Subsequent loss of the protective CD59 antigen may initiate postinjury clearance of the irreversibly damaged tissue.

Animals↗