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Immunoglobulin gene expression in rheumatoid arthritis
S L Bridges1, W J Koopman, S K Lee
1University of Alabama at Birmingham, USA.
Agents and Actions. Supplements
|January 1, 1995
Summary
Rheumatoid arthritis (RA) involves inflammation driven by antigen stimulation, leading to immunoglobulin production in the synovium. This suggests abnormal B cell selection may contribute to RA pathogenesis.
Area of Science:
- Immunology
- Rheumatology
- Molecular Biology
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting the synovium.
- Immunoglobulin-secreting plasma cells are present in RA synovium, but the drivers of this expression are unclear.
Purpose of the Study:
- To investigate the forces driving immunoglobulin expression in rheumatoid arthritis (RA) synovium.
- To explore the B cell response in RA synovium at the molecular level.
Main Methods:
- Analysis of VH and VK transcript sequences from an RA synovial cDNA library.
- Examination of patterns of somatic mutation and B cell repertoire.
Main Results:
- Synovial immunoglobulin expression in RA appears to be driven by antigen stimulation.
- Evidence suggests an oligoclonal B cell response, with 5% of the kappa repertoire originating from a single progenitor.
- The RA synovium shows enrichment for unusually long VK-JK joins (CDR3s).
Conclusions:
- Immunoglobulin expression in RA synovium is likely a result of antigen stimulation.
- Abnormal selection or regulation of the B cell response, indicated by long CDR3s, may play a role in RA pathogenesis.