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Antilymphocyte antibodies in progressive systemic sclerosis.
Clinical and Experimental Rheumatology
|January 1, 1983
Summary
Scleroderma patients often have cold-reactive antilymphocyte antibodies (ALA) targeting T cells. These antibodies show varied binding, suggesting potential roles in disease pathogenesis requiring further study.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Scleroderma is an autoimmune disease characterized by fibrosis of skin and internal organs.
- Immunological abnormalities are frequently observed in scleroderma patients.
- The presence and specificity of antilymphocyte antibodies (ALA) in scleroderma remain incompletely understood.
Purpose of the Study:
- To investigate the presence and characteristics of antilymphocyte antibodies (ALA) in patients with scleroderma.
- To determine the specificity of detected ALA, particularly against T cells.
- To explore the potential relationship between ALA and the UCHT1 receptor on T cells.
Main Methods:
- Sera from 19 scleroderma patients were analyzed using indirect immunofluorescence assay.
- Antibody binding was assessed at different temperatures (0°C and 25°C).
- B and T cells were separated to determine antibody specificity, and a monoclonal antibody (UCHT1) was used to probe T cell receptors.
Main Results:
- Antilymphocyte antibodies (ALA) were detected in 47% of patients at 0°C and 27% at 25°C.
- Separation of lymphocytes confirmed anti-T cell specificity for the detected ALA.
- Significant heterogeneity in ALA binding was observed among patients and within individual sera.
- UCHT1 antibody partially or completely inhibited ALA binding in four patients, indicating receptor similarity.
Conclusions:
- Scleroderma is associated with the presence of cold-reactive anti-T cell specific ALA.
- The detected ALA exhibit heterogeneity and target T cells, potentially through receptors similar to the UCHT1 target.
- Further research is warranted to elucidate the pathogenic role of these cold-reactive anti-T cell ALA in scleroderma.