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Biomedical subjects

W Liman

Publications and source records attributed to W Liman.

4 recordsLinked to original sources

Platelets as target cells in rheumatoid arthritis and systemic lupus erythematosus: a platelet specific immunoglobulin inducing the release reaction.

Sera from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were assessed for in vitro platelet activation as measured by serotonin release; 24% (30) of 124 tested RA sera and 51% (35) of 69 SLE sera induced a significant 3H serotonin release. Investigation of 17 synovial fluid samples from RA patients revealed significant release in 82%. Concomitant testing for lymphocytotoxic antibodies and immune complexes did not show any correlation to platelet activation. Upon gel filtration the release-inducing activity of positive sera was localized in the region of 160 000 Daltons. Further characterization by ion exchange chromatography, immune electrophoresis, chromatographic and SDS PAGE molecular weight determinations, as well as analytical ultracentrifugation all confirmed the IgG nature of the release-inducing protein. Negative blocking experiments performed by preincubation of platelets with Fc-IgG fragments prior to challenge with a release-inducing serum excluded the participation of Fc receptors in the reaction. It was concluded that the release was caused by a platelet reactive IgG antibody. This antibody may also cause release of platelet mediators in vivo and may thus contribute to the pathogenesis of the generalized vasculopathy in both diseases.

Adult

Characterisation of blood and synovial fluid lymphocytes from patients with rheumatoid arthritis and other joint diseases by monoclonal antibodies (OKT series) and acid alpha-naphthyl esterase staining.

Mononuclear cell preparations from peripheral blood (PBL) and synovial fluid (SFL) of 27 Patients with rheumatoid diseases (15 patients with definite rheumatoid arthritis (RA), 10 with other inflammatory joint diseases (OJD), 1 with sarcoid arthritis (SA) and 1 with traumatic arthritis (TA) were examined for lymphocyte subpopulations determined by monoclonal antibodies of the OKT series and by the dot-like, acid alpha-naphthyl esterase staining (ANAE) activity. In patients with classic, active RA, blood T cells carrying the OKT8+ (suppressor/killer) phenotype were significantly reduced leading to an elevated OKT4/OKT8 ratio of 4.1 +/- 0.4 compared with 2.1 +/- 0.1 in healthy controls. In 10 patients with OJD this diminution of OKT8+ cells in peripheral blood was less pronounced or absent. As regards SFL subpopulations, patients with RA and OJD exhibited a similar distribution pattern with an elevation of OKT8+, Ia+ and ANAE negative cells and a similar OKT4/OKT8 ratio of 1.5 +/- 0.3 and 1.6 +/- 0.4, respectively. Similar results were also obtained in the only patient with TA, whereas the patient with SA and one RA patient with relapse after surgical synovectomy exhibited high OKT4/OKT8 ratios, both in synovial fluid and peripheral blood. Neither the OKT markers nor the dot-like ANAE staining pattern were significantly correlated to parameters of systemic or local disease activity as estimated by erythrocyte sedimentation rate and a local disease activity index.

Adolescent

Immune complexes in multiple sclerosis: relation to clinical pattern.

Using a C1q binding test, circulating immune complexes (IC) were detected in 33.3% of sera from 138 patients and in 19.4% of 124 spinal fluid samples from patients with multiple sclerosis. Most often they occur in sera alone. As a rule their detectable amount is small in sera as well as in spinal fluids. IC were observed with equal frequency during acute exacerbations and in stable phases of the disease. In patients with early MS of less than 3 months duration, IC were detected only rarely, whereas their frequency increased up to 50% in patients with longer standing disease. Immunosuppressive therapy has no influence on IC formation. Patients with immune complexes exhibited a more rapid clinical deterioration if compared as a group with IC-negativ ones. No correlations were found between immune complex formation and the CSF-IgG index or the rate of pleocytosis in spinal fluids. Neither the complement factors C3, C4, C3A nor total hemolytic complement activities (CH50) in serum were significantly decreased in patients with IC formation in serum as compared with the IC-negative group. The results demonstrate that IC formation probably is of no importance in the pathogenesis of multiple sclerosis.

Acute Disease

[(Fab')2-antiglobulins in serum and synovial fluid in patients with chronic polyarthritis].

In addition to the well-known rheumatoid factors or antiglobulins belonging to different immunoglobulin classes, a new type of antiglobulin has been found in serum and synovial fluid from patients with rheumatoid arthritis. 15/20 sera and 6/6 synovial fluids contained serologically active material with a molecular weight of approximately 95.000 Daltons. Using chromatographic and affinity chromatographic methods as well as specific precipitation techniques, the (Fab')2 character of these antiglobulins could be ascertained. These antiglobulins may arise through enzymatic degradation of IgG or monomeric IgM antiglobulins, or may be the product of partial intracellular degradation of phagocytosed immune complexes with subsequent extrusion of such material. An in vitro blocking effect of (Fab')2 type antiglobulins on SCMC or ADCC reactions was not found.

Adult