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Results for “Complement Pathway, Classical”

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At least 1,171 records · Page 65Linked to original sources
PubMed2003

[Study of polymorphism of Fc gamma IIa receptors in Chilean patients with systemic lupus erythematosus].

BACKGROUND: Polymorphisms of Fc receptors for IgG (Fc gamma R) have been proposed as a genetic factor that influences susceptibility for systemic lupus erythematosus (SLE). Human Fc gamma RIIa has 2 codominantly expressed alleles, H131 and R131, which differ at amino acid position 131 in the second extracellular domain (histidine or arginine respectively) and differ substantially in their ability to bind human IgG2. The H131 allele binds IgG2 efficiently, whereas R131 binds it poorly. Because IgG2 is a poor activator of the classical complement pathway, the H131 is essential for the disposal of IgG2 immune complexes. AIM: To determine the distribution of Fc gamma RIIA genes in a cohort of Chilean SLE patients, with or without a history of lupus nephritis. PATIENTS AND METHODS: We studied 52 Chilean SLE patients fulfilling the 1982 American College of Rheumatology (ACR) criteria, 20 of whom had a history of nephritis, and 44 ethnically matched disease-free controls. Fc gamma RIIa allotypes were genotyped by PCR. RESULTS: No significant association was observed between the low affinity Fc gamma RII receptor (FcgRIIa-R131) and the presence of SLE or lupus nephritis. However, genotype frequencies in SLE patients but not in controls, departed from the proportions predicted by the Hardy-Weinberg equilibrium, suggesting this locus might be related to the disease. CONCLUSIONS: Our results suggest that in Chilean patients with SLE, as well as in many other populations, the R131 allotype is not a major factor predisposing to the development of SLE or lupus nephritis.

Alleles↗
PubMed1992

[Complement system in status asthmatics--analysis of anti-complementary effects induced by methylprendisolone].

Complement system was investigated in 7 patients with status asthmatics treated with large doses of methylprednisolone (MPS). Complement hemolytic activities, complement protein profile, complement fragments and circulating immune complexes were measured before, 3 and 8 hours after and 14 days after MPS administration. MPS normalized C4 and C1INH activities 6 hours after administration. MPS also decreased ACH50 6 hours after administration and D activity 3 and 6 hours after, but these activities recovered to their previous normal range within 14 days. P and H were decreased at each measurement time, and C1s was transiently decreased 6 hours after MPS administration. Complement fragment iC3b was increased at each measurement time, but fragment Bb tended to be decreased 14 days after MPS administration. The increment of anaphylatoxin C3a recovered to normal 14 days after MPS administration. In vitro experiments, MPS inhibited D and C1s activation directly, and decreased the decay of B and C4. Inhibition of C1s might also increase C1INH activity clinically. These results clarified that the alternative complement pathway was activated, and suggested that the C1 bypass pathway might be also activated in status asthmatics. It was further considered that these anti-complementary effects induced by MPS, brought about an improvement in asthmatic symptoms. Studies to identify the complement activators continued, and circulating immune complexes may possibly be one of those agents activating complement cascade.

Adult↗
PubMed1992

Plasma histamine but not anaphylatoxin levels correlate with generalized urticaria from infusions of anti-lymphocyte monoclonal antibodies.

Anti-lymphocyte monoclonal antibodies have shown promise in trials for therapy of lymphocyte malignancies but are associated with a high frequency of immediate-type anaphylactoid reactions. We have previously demonstrated that these immediate-type anaphylactoid reactions are not mediated by immunoglobulin E to anti-lymphocyte monoclonal antibodies. To gain insight into the mechanisms of these immediate-type anaphylactoid reactions, we measured plasma levels of histamine and anaphylatoxins (C3a, C4a, C5a) during 11 infusions in eight patients who received anti-lymphocyte monoclonal antibodies (T101 and Lym-1). Three patients experienced generalized urticaria (two with severe angioedema); a fourth patient had three isolated hives but without generalized manifestations of an immediate-type anaphylactoid reaction. Plasma histamine levels after infusions that were associated with generalized urticaria were significantly higher than those during infusions that were not associated with generalized urticaria (mean, 3.47 vs 0.18 ng/ml, p less than 0.001). Increases in C3a and C4a levels were observed after some infusions, but these did not correlate with generalized urticaria. Measurable rises in plasma C5a levels after infusions were not detected. Although these data should be viewed as preliminary considering the limited number of patients studied, the observed histamine release demonstrates that mast cell or basophil activation that is not mediated by immunoglobulin E to anti-lymphocyte monoclonal antibodies occurs in the pathogenesis of immediate-type anaphylactoid reactions from anti-lymphocyte monoclonal antibodies. Although activation of the classical complement pathway may occur in some anti-lymphocyte monoclonal antibody infusions, this does not appear to explain immediate-type anaphylactoid reactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylatoxins↗
PubMed2004

[C-reactive protein and atherosclerosis].

Human C-reactive protein (CRP) is an acute phase protein which arises rapidly and tremendously in serum when the subject is exposed to infection and tissue injury. CRP can effectively opsonize by both activating the complement classical pathway and potentiating the phagocytosis of phagocytes, thus clearing the invading pathogens and tissue cells undergoing injury, necrosis and apoptosis and performing an important protective role in the innate immune system. It has been over 70 years since CRP was first discovered. Traditional wisdom holds that CRP is a non-specific marker of inflammation. However, accumulating evidence during the last decade has elucidated that CRP, plays a direct role in the inflammation and cardiovascular disease such as atherosclerosis and can be recognized as the most powerful risk factor and predicator of cardiovascular disease, hence at present receiving attention worldwidely.

Acute-Phase Reaction↗
PubMed2005

The effect of glycation of CD59 on complement-mediated cytolysis.

Vascular proliferation is one of the major causes for morbidity and mortality in diabetes. However, the cellular and molecular mechanisms that link hyperglycemia to this complication remain unclear. In present study, we demonstrated by site-directed mutagenesis that mutated CD59 was more susceptible to glycation-inactivation for hyperglycemia. Mutated and wild-type CD59s were stably expressed in Chinese hamster ovary cells using the pALTER-MAX mammalian expression vector. Western blot, FACS and immunological fluorescence were conducted to confirm that CD59s were tethered to the plasma membrane. Compared to wild-type CD59, human CD59 mutants led to a significant increase in dye release assay. These results indicate that there may be some mutations of CD59 in diabetes population and the mutated CD59, which is more likely to be of glycation than the wild-type, may help to explain the distinct propensity of diabetes subjects to develop vascular proliferation complications.

Animals↗
PubMed2005

Complementing the patient: a complement component deficiency in a patient with recurrent infections and glomerulonephritis.

We present a case showing the investigation of a 7-year-old girl with empyema and glomerulonephritis whose "immunological" defect was a single complement component (C2) deficiency which prevented her from activating her classical complement pathway. A defect in complement function should be suspected in any patient with severe or recurring pyogenic infections. Investigations of "? immune deficiency" should always include tests to assess the patency of the patient's complement system.

Child↗
PubMed1991

Elisa for the measurement of complement C3 activation by autoantibodies directed against thyroid membrane antigens.

This paper describes the use of an ELISA technique to assess the involvement of the complement system in the pathogenesis of autoimmune thyroid disease (AITD). Microtitre plates coated with thyroid membrane antigen were exposed to serum samples obtained from AITD patients, all of whom showed elevated levels of circulating anti-thyroid autoantibodies, and dilute guinea pig serum, as a source of complement, was then added to the microtitre wells. The degree of activation of the classical complement pathway was assessed by measuring the bound complement component C3 using a peroxidase conjugated anti-guinea pig C3 antiserum. C3 fixation and activation was greater in the presence of serum from patients with Hashimoto's disease when compared with that seen in patients with autoimmune hyperthyroidism (Graves' disease). Serum samples obtained from normal healthy volunteers and from patients with thyroid neoplasia were negative in this assay. The method allows the calculation of a putative "biologically active autoantibody" level and analysis of these data confirm our earlier observation that the species of autoantibody found in autoimmune hypothyroidism are potentially more destructive than those found in other forms of AITD.

Animals↗
PubMed1977

Effect of heparin on complement activation and lysis of paroxysmal nocturnal hemoglobinuria (PNH) red cells.

The effect of heparin upon the binding of the third component of complement (C3) to PNH red cells in vitro and their subsequent hemolysis is described. Heparin, in increasing concentrations, progressively inhibits membrane C3 fixation and hemolysis when the classic complement pathway is activated by anti-red cell antibodies. Heparin has a biphasic effect upon membrane C3 fixation and hemolysis when complement is activated in serum at decreased ionic strength (sucrose lysis) or in serum at decreased pH (Ham test). Heparin in concentrations above 2 U/ml inhibits C3 binding and hemolysis while lower concentrations of heparin enhance the consequences of complement activation by these two procedures. This enhanced complement activation may explain the increased hemolysis sometimes reported in PNH patients treated with heparin, and suggests that heparin may aggravate the consequences of pathologic alternative pathway complement activation in other diseases.

Binding Sites, Antibody↗
PubMed1991

Inhibition of complement activity in murine leprosy.

NIH mice infected with Mycobacterium lepraemurium (MLM) show a marked depression in their levels of hemolytic complement that is proportional to the degree of infection. The defect affects more the activation of complement through the classical pathway (CPW) than the activation of complement through the alternative pathway. Although this low activity of CPW-complement may be due to different causes (complement consumption by the infecting microorganism, lack of biosynthesis of complement components, or the presence of complement inhibitory factors), our results seem to support the last possibility. The generation of factors in the infected animals that inhibit the autologous activity of complement as the infection goes on reduces the risk of complement-mediated tissue damage and prolongs the survival time of the host, a wise strategy on the part of the MLM to assure its own survival as a parasite.

Animals↗
PubMed1991

Isolation and partial characterization of circulating immune complexes in sera of children with HBV-mediated glomerulonephritis.

Circulating immune complexes (CIC) containing HBsAg and HBeAg were identified in sera of 5 out of 6 children with hepatitis B mediated membranous glomerulonephritis. CIC were precipitated from sera by 3.5% PEG, washed and subsequently analysed after acid dissociation and trypsin digestion. HBsAg, anti-HBs and albumin; HBeAg, anti-HBe and anti-HBc were recovered from the isolated complexes and these findings are discussed. Analysis of 3.5% PEG mediated precipitate of human serum proteins showed the relatively high content of IgG classical pathway complement components: C1q, C4 and C3.

Adolescent↗
PubMedDate not supplied

Immunological alterations following open heart surgery.

Immunological changes in thirty patients undergoing various cardiac surgical procedures (twenty patients undergoing open heart surgery with either the bubble or the membrane oxygenator and ten patients undergoing closed surgical procedures) were studied. There was an activation of suppressor T cells and secretion of lymphokines in patients undergoing open heart surgery with activation of the classical complement pathway. The immunological alterations were similar in all patients irrespective of the type of oxygenator used.

Adolescent↗