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At least 415 records · Page 23Linked to original sources
PubMed1976

Multiple immune complexes and hypocomplementaemia in dermatitis herpetiformis and coeliac disease.

Circulating immune complexes have been detected in 100% of 59 patients with dermatitis herpetiformis (D.H.), and in 100% of 27 patients with coeliac disease (C.D.). Three methods for detecting immune complexes were employed: radiobioassay, which gave an incidence of 77% in D.H. and 81% in C.D.; C1q binding activity, with which the incidence was 83% and 96%, respectively; and precipitation with 4% polyethylene glycol (69% positivity in D.H., 100% in C.D.). The immune complexes in D.H. and C.D. were compared with those in sera from 23 patients with systemic lupus erythematosus (S.L.E.). Multiple complexes of differing properties were found in D.H. and C.D. but not in S.L.E. The varying nature of the complexes in D.H. and C.D. may account for the damage to different tissues (skin, small intestine, reticuloendothelial system). Low third component of complement was found in 49% and low C4 in 20% of D.H. patients. C3 hypocomplementaemia was found in 26% of patients with C.D.

Adult↗
PubMed1976

Evidence for immune-complex formation in patients with amyotrophic lateral sclerosis.

Immune complexes have been found in several chronic diseases of unknown aetiology and identification of the constituents of the complexes might lead to recognition of aetiological agents. Sera and renal tissues from patients with amyotrophic lateral sclerosis (A.L.S.) were studied for evidence of immune complexes. C1q precipitation testing demonstrated that sera from 10 of 25 patients with classic A.L.S. bound significantly more radiolabelled C1q than sera from 15 controls. In renal glomeruli studied for deposition of host 1gG, C3, fibrinogen, and albumin by means of direct immunofluorescence, 9 of 33 patients with A.L.S. (27 biopsy and 6 necropsy specimens) had moderate amounts of both IgG and C3 of granular basement membrane and mesangia. This pattern of immunofluorescence is characteristic of immune complex deposits. Of these 9, 8 had rapidly progressive neurological courses, whereas among the remaining 18 patients with no evidence of immune-complex disease, 9 of 12 available for clinical follow-up had stable or slowly progressive courses.

Amyotrophic Lateral Sclerosis↗
PubMed1976

Plasmapheresis in the management of acute systemic lupus erythematosus?

Eight patients with systemic lupus erythematosus (S.L.E.) have been treated with plasmapheresis. In four patients in whom immunochemical studies indicated high levels of circulating immune complexes, the removal of 5-8 litres of plasma weekly produced a striking clinical and immunochemical improvement. The four other patients, with only minor complement disturbances and no direct evidence of circulating immune complexes, could not be shown to benefit from plasmapheresis and one patient in this group died of cerebral lupus despite intensive treatment with cytotoxic drugs. It is concluded that plasmapheresis may be of value as an adjuvant to the treatment of acute S.L.E.

Acute Disease↗
PubMed1977

Is primary biliary cirrhosis an immune complex disease?

Large immune complexes are present in the circulation of patients with primary biliary cirrhosis and result in the activation of complement by the classical pathway. Such large complexes are capable of producing tissue damage. The granulomatous lesions surrounding the small bile-ducts within the liver of patients with primary biliary cirrhosis and the vasculitis, rheumatoid arthritis, and associated lesions are all compatible with immune complex injury. It is postulated that such large complexes could be formed in the vicinity of the bile-ducts by an antigen absorbed from the bile or biliary epithelium. Complexes reaching the systemic circulation might be responsible for the associated extra-hepatic diseases.

Antibody Formation↗
PubMed1977

Complement activation in migraine.

Forty patients attending the Prince Henry Hospital migraine clinic have been investigated for evidence of complement activation related to migraine. These patients had a history of clinically similar migraine attacks. Levels of serum complement components were determined in nine patients, both in and out of migraine. Comparison of these levels showed significant reductions in C4 and C5 during headache. In a further 31 patients C3 breakdown products were sought when these patients were headache-free. They were detected in the plasma of three patients who proceeded to a migraine attack but not in the plasma of the remaining twenty-eight who did not. These findings suggest the presence of complement activation, which could explain many of the previously reported phenomena associated with migraine.

Complement C1↗
PubMed1978

Value of immune-complex assays in diagnosis and management.

Two complement-dependent assays for circulating immune complexes, the C1q-binding assay and the conglutinin binding, were used to study patients with suspected immune-complex disease. Complexes were detected most frequently in multisystem disease such as infective endocarditis (69%) and systemic lupus erythematosus (60%), and less frequently in isolated nephritis (26% of membrano-proliferative nephritis). Sequential estimations in 32 patients showed that concentrations of circulating immune complexes correlated with disease activity and were useful in monitoring therapy.

Adolescent↗
PubMed1998

Complement activation and CD59 expression in the motor facial nucleus following intracranial transection of the facial nerve in the adult rat.

Intracranial transection of the facial nerve has been shown to cause a massive neuronal cell death in the motor facial nucleus. Complement activation has been proposed to contribute to neuronal degeneration following axotomy. Using immunocytochemistry and in situ hybridization we show in the present study that there is complement activation in the facial nucleus after intracranial facial nerve transection as well as increase of the complement regulators CD59 and clusterin. We propose a neuroprotective role for the complement regulators CD59 and clusterin against homologous attack of complement to facial motor neurons.

Age Factors↗
PubMed1987

Complement activation in patients with amebic liver abscess.

Serum or plasma concentrations of components of the classical (C1q, C4) and alternative (C3, factor B) pathways, regulatory protein factor H, and one of the C3 products of degradation, C3d, were determined in 19 patients with amebic liver abscess (ALA). Patients were divided into two groups. Thirteen patients that recovered under medical treatment who had a significantly shorter clinical course on admission (P less than 0.05) (group 1) exhibited either normal (C1q; C4; factor B; C3d) or increased levels of these components (C3, P less than 0.001; factor B, P less than 0.01). On the other hand, 16 patients that recovered after medical treatment and abscess drainage (group 2) exhibited significantly diminished serum levels of C1q (P less than 0.05), C3 (P less than 0.001), factor B (P less than 0.01) and factor H (P less than 0.05), and normal levels of C4, and C3d as compared to the control group. The relationships among the complement components studied were suggestive of activation of the complement system through the classical pathway in patients within group 1 and through both pathways in group 2. Sera of 3 out of the 5 patients who initially exhibited low plasma levels of C3d showed an increase during convalescence. Plasma levels of C3d were demonstrated to show a direct correlation with serum albumin and SGOT in this group of patients. Possible implications of the complement system in the immunopathogenesis of ALA are discussed.

Complement Activating Enzymes↗
PubMed1980

Evidence that C1q, a subcomponent of the first component of complement, is an Fc receptor of peritoneal and alveolar macrophages.

Guinea pig peritoneal macrophages were cultured for 24 h in the presence of two inhibitors of the biosynthesis of collagen-like molecules such as C1q : 10(-3) M 3,4-dehydroproline or 10(-4) M 2,2'-dipyridyl. Their Fc-receptor activity was measured by rosette formation, using sheep erythrocytes (E) coated with rabbit anti-sheep IgG (EAIgG). The Fc-receptor activity was decreased by 40 to 70% of control cultures depending on the amount of IgG on the E. The activity of a second receptor on the macrophages, mediating the binding of C3b coated E, was not altered by this treatment. Rat alveolar macrophages were depleted of their Fc-receptor activity by pronase treatment (1.5 mg/ml) in the presence of 2,2'-dipyridyl. After washing the cells, the EAIgG-binding activity was restored to about half of the initial level within 2 h. With 2,2'-dipyridyl also present during the second incubation, the re-expression of the Fc-receptor activity was suppressed further. Preincubation of guinea pig peritoneal macrophages with anti-C1q-F(ab')2 for 45 min at 37 degrees C caused a dose-dependent reduction of the Fc receptor activity, but not C3b receptor activity. These results support our hypothesis that C1q synthesized and secreted by macrophages serves as an Fc-receptor in the membrane during the secretion.

2,2'-Dipyridyl↗