Abstract / Description of output
Immunodominant antigens in rheumatoid arthritis (RA) should induce an expansion of T cells bearing a corresponding T-cell receptor (TCR). We therefore analysed the TCR repertoire at the site of inflammation using two fundamentally different strategies. The total TCR repertoire was examined by generating 'representative' T-cell clone panels, which were subsequently tested for clonality by restriction mapping of the TCR beta gene locus. No clonality was detected in large T-cell clone panels generated with cells from three patients. However, when we selectively analysed the TCR repertoire of in vivo pre-activated, interleukin-2 (IL-2)-responsive T cells, significant T-cell/TCR clonality was found in 2 out of 4 patients. The clonal T cells represented a minority of the total T-cell population with an estimated frequency of 1 in 300 to 1 in 1000 cells. Molecular characterization of a clonal TCR and the use of a specific TCR V beta MoAb ruled out an over-representation of T cells bearing the same V beta element in the total T-cell population, rendering the involvement of super-antigens in the induction of T-cell clonality in this case unlikely.
Original language | English |
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Pages (from-to) | 855-63 |
Number of pages | 9 |
Journal | Scandinavian Journal of Immunology |
Volume | 36 |
Issue number | 6 |
Publication status | Published - Dec 1992 |
Keywords / Materials (for Non-textual outputs)
- Amino Acid Sequence
- Arthritis, Rheumatoid
- Base Sequence
- Blotting, Southern
- Clone Cells
- Cloning, Molecular
- Flow Cytometry
- Humans
- Molecular Sequence Data
- Polymerase Chain Reaction
- Polymorphism, Restriction Fragment Length
- Receptors, Antigen, T-Cell, alpha-beta
- Synovial Fluid
- T-Lymphocytes