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At least 847 records · Page 47Linked to original sources
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

Immune complexes in patients with drug eruptions: the relationship between skin lesions and circulating immune complexes.

The relationship between skin lesions and immune complexes was studied in sixty-two patients with exanthematic drug eruptions. By means of C1q-binding, conglutinin-binding and platelet aggregation tests, immune complexes were detected in a considerable number of sera from these patients. Patients with widespread maculopapular drug eruptions were found to show a relatively high serum level of immune complexes. There was a close association between the disease activity and the amount of the circulating immune complexes. By immunofluorescence, six of seventeen patients with drug eruptions were shown to have deposits of IgG, IgM, IgA or C3 in the skin lesions. These results suggest that certain immune complexes may play a role in some types of drug eruption as a pathogenetic factor.

Antigen-Antibody Complex↗
PubMed1980

Articular complications of meningococcal meningitis. An immune complex disorder.

A case of noninfectious arthritis was associated with meningococcal meningitis. Elevated levels of immune complexes were demonstrated in both serum and synovial fluid by the C1q binding assay and Raji cell assay. We believe this complication of meningococcal infection is another disorder in which immune complexes may play a pathogenic role.

Adult↗
PubMed1984

[Binding and activation of the first component of human complement on artificial matrices].

Artificial sorbents that comprise macroporous glass covered by the copolymer of N-vinylpyrrolidone and N-substituted acrylamide have been synthesized. Aminoethanol is bound to acrylic acid residue in one sorbent (AE-glass), whereas the other sorbent involves immunoglobulin G with the hexamethylenediamine spacer (IgG-glass). C1q binds specifically to IgG-glass with Ka 4,07(+/- 0,32) X 10(7) M-1. Free energy of the C1q binding to IgG-glass is twice higher than that of its binding to monomeric IgG. This evidences that one C1q molecule associates with two IgG molecules of the sorbent. A weak nonspecific sorption of C1q to AE-glass was found. Both specific (on IgG-glass) and nonspecific (on AE-glass) sorption of the first component of complement activate the classical pathway in human serum as manifested in the consumption of the C4, C2, C3 and C5 components. IgG-glass was employed for C1q isolation from human serum by affinity chromatography, whereas unbound part of serum may be used as a reagent R1q. The yield of highly purified C1q after IgG-glass affinity chromatography and gel filtration on Sephacryl S-300 is 63,6%.

Chemical Phenomena↗
PubMed1984

Exacerbation reactions in hyperactive lepromatous leprosy.

Exacerbation reactions (ER) are acute reactions occurring locally in histoid or other highly active lepromatous lesions with an exceptionally heavy bacterial load. Clinically, they are almost silent although they may cause ulceration and the release of viable bacilli. Histologically, the influx of polymorph neutrophils and coincident macrophage degeneration mimic erythema nodosum leprosum (ENL). Later, the signs of increased permeability or necrosis of small blood vessels and mast cell degranulation are differential features. The predominant immunoglobulin is IgE, and the main complement component is C1q, C3 being mostly undetectable. The reactions appear to be mediated in part by reagins (although eosinophils are not seen). Immune complexes probably form at antigen excess. Of equal importance may be the release from highly activated macrophages and neutrophils of hydrolases and proteases, which are capable of degrading connective tissue and other cell surfaces. This report is based on a histopathological and an immunocytological study of 13 exacerbation reactions in comparison with nonreacting hyperactive lesions and with ENL. The results support the view that the essential feature of histoid lesions is their hyperactivity.

Complement C1↗
PubMed1983

Complement polymorphism, the major histocompatibility complex and associated diseases: a speculation.

Genes in the major histocompatibility complex code for three major groups of glycoproteins, now referred to as classes I, II, and III. Susceptibility to some autoimmune diseases and to systemic lupus erythematosus is associated with the presence of particular haplotypes of genes in these three classes. An attempt has been made to correlate these finding on the basis of the observation that different polymorphic forms of complement component C4 show varying efficiencies of complement activation. It is suggested that susceptibility to these diseases will be related to the varying efficiency of complement cell lysis and of immune aggregate dissolution by complement. This in turn will depend on the strength of interaction of the different polymorphic forms of C4 with other proteins (some also polymorphic) in the scheme of activation and inactivation of complement. Such an arrangement would lead to preferential association of certain alleles of C2, C4 and factor B and possibly also of class I and II antigens as potential targets of complement reaction.

Animals↗