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Biomedical subjects

U Nydegger

Publications and source records attributed to U Nydegger.

54 records · Page 3Linked to original sources
PubMed1979

[Alternative complement pathway (author's transl)].

The dual role of the alternative complement pathway in recognition of foreign substances by a non-immune host and in the intrinsic regulation of the complement sequence is now well recognized. Activation of this pathway occurs through escape from its regulatory mechanisms induced by the activating principle; its functional expression depends on the respective levels of the component proteins C3, factor B, factor D and properdin, and on the control proteins beta 1H and C3bINA. This article presents recently acquired knowlege on the molecular mechanisms of activation, regulation and behaviour under pathological conditions of the alternative complement pathway.

Complement Activation↗
PubMed1979

[The detection of soluble immune complexes (author's transl)].

The detection and characterization of soluble immune complexes is complicated by the broad spectrum of complexes occurring in human pathology. Thus, differences in immune complex size, specificity and ability to interact with immunologic effector systems such as complement or cells, suggest variable pathogenic potential. Therefore, a variety of techniques for detection should be available. The introduction of radioimmunoassays and the recently improved knowledge of immune complex biochemistry have lead to the description of a large number of detection procedures, which in turn has widened the catalogue of diseases associated with immune complexes. Among 50 procedures known today, this article selects some pertinent tests which are critically discussed with respect to their specificity, sensitivity and possible interest in clinical medicine.

Antigen-Antibody Complex↗
PubMed1979

Complement activation in pneumonia.

Complement analyses performed on serially collected plasma samples from 10 patients during acute infectious pneumonia or bronchopneumonia showed normal or increased values for hemolytic activity and Clq, C4, C3, and factor B levels. However, the levels of C3 breakdown products (C3d) were significantly (greater than 2 SD) increased in six patients during the first three days of observation, suggesting that hypercatabolism of complement components may occur during the acute phase of infectious pneumonia concomitant with a hypersynthesis of some complement components. Evidence of circulating immune complexes was obtained only in two patients with the 125I-Clq Binding Test.

Acute Disease↗
PubMed1979

Immune complexes and complement in rheumatoid arthritis.

Immune complexes have been shown to occur frequently during rheumatoid arthritis. They have been found in blood, in the synovium and in other extravascular lesions. The recent development of methods for the quantitation of immune complexes provided new tools to evaluate the possible role of immune complexes in rheumatoid arthritis. Immune complexes which appear in synovial fluid are in higher concentration than in serum and have particular physicochemical properties. They likely result from a local formation in the synovium and seem to be directly involved in the generation of the local inflammation. High levels of circulating immune complexes are usually associated with the development of extra-articular vascular lesions. One of the major biological activity of immune complexes is to activate the complement system. There is indeed evidence of complement activation in circulating blood as well as in synovial fluid in patients with rheumatoid arthritis. The presence and the concentration of complement breakdown products in these fluids correlates with the clinical activity. Therefore, the analysis of immune complexes and of complement components appears useful for diagnosis and follow-up, and for the understanding of the pathogenesis of the disease.

Antigen-Antibody Complex↗
PubMed1978

[Cutaneous plasmacytosis and polyclonal cryo-immunoglobulinemia].

A 65-year-old male patient is described who presented with (1) large violet cutaneous plaques on the left side of the body, characterized by dense plasmocyte infiltration of the dermis which appeared benign and largely negative to immunofluorescence, (2) massive polyclonal cryoglobulinemia (type III) without paraproteins, and (3) intermittently marked peripheral monocytosis and thrombopenia without significant medullary changes. Compared with the cases reported in the literature, and after a thorough immunological investigation, this syndrome cannot be entirely assimilated to any entity described up to the present time. Hypothetically, a reactional disorder is the most likely.

Aged↗
PubMed1977

[Evaluation of the role of circulating antigen-antibody complexes in the pathogenesis of glomerular nephropathies].

Immunofluorescence studies of the glomeruli in patients suffering from glomerulonephritis (GN) suggest the deposit of immune complexes from the circulating blood. Immune complexes were quantitated using a sensitive radioimmunoassay from sera of 41 patients with GN drawn at the time when renal biopsy was performed. Simultaneously, degradation products of C3 (C3d) were measured. Eleven of 12 patients with GN secondary to a systemic disease (usually LED) presented increased C1q-binding activity of their sera (C1q-BA). C3 was further demonstrated in 9 of these patients, suggesting the presence of circulating immune complexes. By contrast only 2 of 12 patients with idiopathic GN characterized by deposits of complement and IgG in the glomeruli exhibited increased C1q-BA. One of 17 patients with idiopathic GN without deposit of immunoglobulins and C3 in the glomeruli also had increased C1q-BA. The results observed in the group of patients with idiopathic GN with glomerular deposits could be accounted for either by a transitory or minimal presence of immune complexes or by local formation of complexes in the glomerular structures.

Antigen-Antibody Complex↗
PubMed1976

Circulating and intra-articular immune complexes in patients with rheumatoid arthritis. Correlation of 125I-Clq binding activity with clinical and biological features of the disease.

The correlation between the incidence and level of immune complexes in serum and synovial fluid and the various clinical and biological manifestations of rheumatoid arthritis has been studied. Immune complexes were quantitated using a sensitive radioimmunoassay, the 125I-Clq binding test, in unheated native sera and synovial fluids from 50 patients with seropositive (RA +) and 45 with seronegative (RA -) rheumatoid arthritis, 17 with other inflammatory arthritis, and 37 with degenerative and post-traumatic joint disease. The following observations were made: (a) when compared to the results from patients with degenerative and post-traumatic joint diseases, the 125I-Clq binding activity (Clq-BA) in synovial fluid was found to be increased (by more than 2 SD) in most of the patients with RA + (80%) and RA - (71%) and in 29% of patients with other inflammatory arthritis; the serum Clq-BA was also frequently increased in both RA + (76%) and RA - (49%) patients, but only exceptionally in patients with other inflammatory arthritis (6%); (b) a significant negative correlation existed between the Clq-BA and the immunochemical C4 level in synovial fluids from patients with RA + and RA -; (c) neither the serum nor the synovial fluid Clq-BA in rheumatoid arthritis significantly correlated with the erythrocyte sedimentation rate, the clinical stage of the disease, or the IgM rheumatoid factor titer; and (d) the serum Clq-BA in patients with rheumatoid arthritis and extra-articular disease manifestations (40 +/- 34% in those with RA +,32 +/- 29% in those with RA -) was significantly increased as compared to the serum Clq-BA in patients with joint disease alone (24 +/- 30% in those with RA +, 10 +/- 13% in those with RA -). Experimental studies were carried out in order to characterize the Clq binding material in rheumatoid arthritis. This material had properties similar to immune complexes: it sedimented in a high molecular weight range on sucrose density gradients (10-30S) and lost the ability to bind Clq after reduction and alkylation, or after acid dissociation at pH 3.8, or after passage through an anti-IgG immunoabsorbant. DNase did not affect the Clq BA. These results support the hypothesis that circulating as well as intra-articular immune complexes may play an important role in some pathogenetic aspects of rheumatoid arthritis. The 125I-Clq binding test may also be of some practical clinical value in detecting patients who have a higher risk of developing vasculitis.

Adult↗
PubMed1975

[Physiopathology of hepatitis B virus infection].

Hepatitis B associated antigen (HB-Ag) may be observed in the serum in subjects either apparently healthy or exhibiting a number of disease symptoms. Its incidence among the Geneva voluntary blood donors is 0.48% with 54% exhibiting the surface antigen ad and 34% ay. While the HB-Ag positive blood donors appeared clinically healthy, minor pathology was found in the majority of them (thrombocytopenia, histological evidence of inflammatory foci, of persistent hepatitis and of chronic aggressive hepatitis). In 82 patients suffering from hepatitis B the same ad-ay type distribution of the HB-Ag has been found. In 11 out of 31 patients increased Clq binding suggests the presence of circulating complexes. Diminutions in the level of complement components also indicates participation of complement in the formation of immunocomplexes. In 2 out of 3 patients with Hb-Ag positive polyarteritis nodosa, the Clq binding test was also positive. The pathophysiologic implications of hepatitis B infection are discussed in connection with the authors and other findings. It appears that the main defense mechanism leading to elimination of the viruses within the hepatocytes lies in cell mediated immunity. Hepatitis would then represent the side reaction of this defense mechanism. Antibodies are probably useful in preventing the virus from entering the cell, but also in the course of the cell mediated defense mechanism (elimination of viral material liberated during the T-cell hepatocellular interaction). Immune complexes may be operative in certain extrahepatic manifestations such as arthralgia. Polyarteritis nodosa may result from local antibody interaction with antigen fixed within arterial walls.

Antibodies↗
PubMedDate not supplied

[Activation of the alternative pathway of human complement (author's transl)].

The C3 amplification convertase of human complement, C3b, Bb, is assembled on biological surfaces by the interaction of the alternative pathway proteins B, D and P with cell-bound C3b. Convertase formation is modulated by the action of the regulatory proteins H and I. On activating surfaces of the alternative pathway, C3b, Bb is relatively resistant to regulation by H. In contrast, non-activating surfaces exhibit surface characteristics such as high content in membrane-associated sialic acid or heparin-related material which increase the interaction of H with cell-bound C3b. Thus, finely tuned molecular interactions allow the alternative pathway to function as a major recognition and effector system for natural defence.

Amino Acid Oxidoreductases↗