PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Complement C4”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,423 records · Page 79Linked to original sources
PubMed1975

Stimulation of neutrophil oxidative metabolism by the alternate pathway of complement activation: a mechanism for the spontaneous NBT test.

The reduction of nitroblue tetrazolium dye by human neutrophils was measured in the presence of serum in which the complement system had been activated through the alternate pathway by interaction with inulin. Neutrophils incubated with serum inulin supernatants reduced the dye and showed a general increase in oxidative metabolism. The oxidation of glucose-1-14-C by supernatant prepared from selectively depleted sera indicated that the neutrophil-stimulating factor(s) was generated through the alternate pathway of complement activation. The possibility that inulun had been ingested as a particle was ruled out by light microscopy and radiolabeling studies. The failure of neutrophils stimulated by the serum-inulun supernatants to migrate after exposure to a chemotactic agent suggested that the site of neutrophil-complement interaction was on the cell membrane. It is concluded from these results that biologically active fragments generated through the alternative pathway of complement activation can stimulate neutrophil metabolism in the absence of phagocytosis. Interaction of such fragments with circulating neutrophils in vivo and the subsequent metabolic activation of these cells is one explanation for the spontaneous reduction of nitroblue tetrazolium dye in vitro by neutrophils from patients with certain infections and inflammatory disorders.

Absorption↗
PubMed1979

Substrate modulation as a control mechanism in the activation of plasma multienzyme systems.

Since plasma is a homogenous fluid its biochemical systems need special control mechanisms to prevent their unlimited and continuous activity. In general, enzymic activity is not preformed but generated by trigger processes. Activation is then enhanced by cascade reactions. It can be controlled by enzyme inhibitors, by enzymes which destroy co-factors, or by spontaneous decay or enzyme complexes involved in the system. In addition, in some reactions of the complement and Hageman factor-dependent systems the necessity of substrate modulation controls the extent of activation. Thus, factor B of the properdin system is activatable by factor D only when bound to the activated third component of complement, and C3b fragment; similarly C2 is activated and forms the C3 converting complex, C42, only when bound to C4b prior to its cleavage by C1; C5 can be activated by either of the two convertases only when bound to surface-fixed C3b; and the mutural activation of Hageman factor and pre-kallikrein on surfaces proceeds efficiently only when HMW-kininogen is present which complexes with pre-kallikrein and possibly with Hageman factor.

Complement C3↗
PubMed1975

The influence of C3b inactivator (KAF) concentration on the ability of serum to support complement activation.

Minor elevation of the concentration of the C3b inactivator (KAF) in whole serum (by 15-25%) markedly inhibits the capacity of the serum to support complement activation by inulin, aggregated IgG and by low concentrations of CVF. However, there was no effect when large concentrations of CVF were used nor was the spontaneous ageing of C3 slowed by increased KAF concentrations. These findings show that the activity of the C3b feedback cycle can be reduced by raising the KAF concentration above physiological levels. This finding may provide a mechanism for damping down complement activation locally in vivo. It seems that the spontaneous ageing of C3 in vitro does not involve a KAF-inhibitable step and therefore cannot be involved to explain the 'C3 tickover' in vitro.

Animals↗
PubMed1979

[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↗
PubMed1977

Immunological studies of human anterior uveitis.

Immunofluorescent studies revealed extracellular deposits of IgG and C3 as well as immunoglobulin containing inflammatory cells in the affected iris of a patient suffering from endogenous acute uveitis. Antibodies to uveal components were detected in the serum of 4 out of a total of 23 endogenous uveitis patients examined. Examination of these 23 sera also revealed antinuclear activity in one, antismooth muscle activity in one, and anti-mitochondrial activity in three. None of the sera showed anti-thyroglobulin activity. Antibodies to uveal components or immune complexes containing 'auto-antibodies' do not appear to be a common source of tissue damage in human endogenous anterior uveitis.

Autoantibodies↗
PubMed1980

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↗
PubMed1980

Evaluation of alternative pathway and factor B haemolytic activities in patients with systemic lupus erythematosus: correlations with the alternative pathway regulatory proteins.

The haemolytic activities of the complement alternative pathway and factor B were studied using a 51Cr-release assay in 77 sera from patients with systemic lupus erythematosus (SLE). These values were compared to those of several complement components and of the regulatory proteins beta H and C3b INA. There was a significant decrease in the alternative pathway activity, which correlated with a decrease in the haemolytic activity of factor B and with the activity of the classical pathway. There was a significant decrease in the level of one regulatory protein beta 1H, while the level of the other regulatory protein, C3b INA, was increased; however, there was a positive correlation between these two parameters. The results obtained suggest that the decreased activity of the alternative pathway observed in SLE reflects a consumption due to a triggering of the C3b amplification loop through the activation of the classical pathway. In one patient, an acquired deficiency of the capacity to activate the alternative pathway in the presence of inulin was observed.

Adult↗