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Results for “Complement Pathway, Classical”

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At least 1,261 records · Page 70Linked to original sources
PubMed1980

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↗
PubMed1982

Selective induction of autoantibody secretion in human bone marrow by Epstein Barr virus.

The bone marrow is an important site for B lymphocyte differentiation and antibody synthesis in animal and man. However, few experiments have examined directly its immunologic functions in humans. In the present experiments, we have induced bone marrow B lymphocytes from human donors with degenerative arthritis of varying ages to secrete two autoantibodies, IgM and anti-IgG (rheumatoid factor) and IgM anti-human thyroglobulin (Tg), by stimulation with the polyclonal B cell activator Epstein Barr virus (EBV). The EBV-stimulated bone marrow cells secreted significantly more IgM anti-IgG (p less than 0.01) and IgG anti-Tg (p less than 0.01) than matched, identically treated peripheral blood cells. Bone marrow cultures from donors over the age of 60 yr, particularly females, produced more rheumatoid factor than cultures from younger donors (p less than 0.01). The EBV-inducible autoantibodies were immunospecific as demonstrated by adsorption studies. A potential pathogenic role in the inflammatory process was suggested by the finding that the EBV-inducible IgM anti-IgG autoantibodies were capable of activating the classical complement pathway as assessed by the cleavage of C4. These results indicate that the human bone marrow is a selective reservoir for EBV-inducible autoantibody precursor B lymphocytes, and that the size of the reservoir increases with age.

Adult↗
PubMed1984

Physiological and pathological effects of activated complement.

In this short review of our present understanding of the complement system the emphasis is on a synopsis of the biological aspects of the various complement components, their fragments and complexes. For this reason we decided to refer to a number of reviews where certain aspects are dealt with extensively.

Anaphylatoxins↗
PubMed1976

Morphological and immunological evidence of coagulopathy in renal complications of pregnancy.

Renal biopsies in 14 patients with P.E.T. or eclampsia showed constant I.F. reactions for IgM and fibrin, with frequent reactions for C1q and C3. The glomeruli showed reversible mesangial proliferation and swelling, with characterictic E.M. deposits, and segmental lesions were present in seven patients. Similar I.F. reactions occurred in three other patients with clinical diagnoses of P.E.T. whose biopsies demonstrated coexistent glomerular disease. Serum complement studies showed a significant rise in C3 in the third trimester of normal pregnancies and a further significant elevation in C1q and C3 in the third trimester of a series of unselected P.E.T. patients. In contrast, four patients from the biopsy series with eclampsia or severe P.E.T. showed profound depression of serum C3 and C4, at the time of maximum clinical severity, which was shown to return to normal in two patients. The I.F. findings confirm those of Petrucco et al (6), and, with the other data, suggest that immune-complex deposition and activation of the classical complement pathway could interrect with intravascular coagulation to produce the glomerular lesions of P.E.T. and eclampsia.

Adolescent↗
PubMed1980

[The complement system and its biological activities].

The complement system is a non specific humoral defence mechanism which can be triggered by various effectors : immune-complexes, extrinsic proteases, bacterial cell-wall polysaccharides, viral membranes. Different peptides or multimolecular complexes are formed by a cascade of proteolytic cleavages; they take an active part in the inflammatory response and may contribute to different pathological manifestations.

Adhesiveness↗
PubMed1981

Hypocomplementaemia due to a genetic deficiency of beta 1H globulin.

An 8-month-old Asian boy who presented with the haemolytic uraemic syndrome was found to have a low haemolytic complement, and in particular a very low C3 level, with a normal C4 level. These abnormalities persisted after recovery and were not associated with the presence of circulating C3 nephritic factor. A clinically healthy 3-year-old brother was found to have an identical complement profile, which indicated increased alternative pathway activation. Both brothers had normal levels of the C3b inactivator, but very low levels of beta 1H globulin (less than 10% of a reference standard serum). The parents, who were first cousins, had half-normal levels of beta 1H globulin, and low levels were found in other members of the family, indicating that the defect was inherited.

Child, Preschool↗
PubMed1984

Immunological mechanisms of reactions to macromolecular solutions.

Hypersensitivity reactions to intravenous macromolecular solutions are an exacerbation of the organism defence mechanisms with production of exaggerated and deleterious effects. The immediate adverse reactions to drugs (anaphylaxis) have clinical manifestations-due to histamine release principally: cutaneous (rash, urticaria, edema); pulmonary (bronchospasm), and cardiovascular (hypotension, collapse, cardiac arrest); their intensity may be graded in degrees I to V. These reactions may be either truly anaphylactic (immunological): hypersensitivity type I with reaginic antibodies (IgE), requiring previous exposure to the drug (true allergy); other immune responses with antigen-antibody (IgG or IgM) complexes activating classical complement pathway; or anaphylactoid; indirect histamine release by direct activation of C3 (alternate complement pathway) direct histamine release by pharmacological effect; dose related effects. The incidence of reactions to plasma substitutes vary greatly according to authors. In most cases, gelatin derivatives act by direct action on mast cells (histamine release) and indeed prevention of reaction with antihistamines is effective; antibody related reactions occasionally occur (immune complexes). With dextrans, soluble immune complexes aggregates have been described; dextrans may react to specific antibodies (possibly previously produced by bacterial polysaccharides); complement activation occur only in severe reactions. HES is comparable to dextran, antibodies have been described. Other factors may predispose to anaphylactoid reactions such as genetic factors (atopy, primary complement anomalies) underlying immune processes and stress. All macromolecular solutions carry the risk of anaphylactoid side-reactions, the mechanisms of which are not completely clarified.

Anaphylaxis↗
PubMed1983

Complement levels in normal and inflamed aqueous humor.

C2, C6, and C7 were measured by hemolytic assay and Factor B and IgG were measured by radial immunodiffusion in samples of normal and inflamed aqueous humor. Normal aqueous humor was found to contain functional C2, C6, and C7, but the small ratios of aqueous humor to serum measurements suggested that there was relatively little of these complement components in normal aqueous humor when compared to serum. The mean values of C2, C6, C7, and Factor B in aqueous humor and the median ratios of aqueous humor to serum measurements for each complement component were higher in patients with inflamed aqueous humor than in patients with normal aqueous humor. A comparison of the ratios of IgG to each complement component in normal and inflamed aqueous humor suggested that levels of IgG and complement increased proportionately in inflamed aqueous humor. Factor B, a component of the alternative pathway, was not detected in normal aqueous humor but measured in five of six samples of aqueous humor from eyes with anterior chamber inflammation.

Adult↗