T-cell receptor gene usage in patients with fibrosing alveolitis and control subjects
P. A. Lympany
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorA. M. Southcott
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorC. M. Black
Royal Free Hospital, Rowland Hill Street, London NW3 2PF, UK,
Search for more papers by this authorR. M. Du Bois
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorP. A. Lympany
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorA. M. Southcott
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorC. M. Black
Royal Free Hospital, Rowland Hill Street, London NW3 2PF, UK,
Search for more papers by this authorR. M. Du Bois
Imperial College of Science, Technology and Medicine, Manresa Road, London, UK,
Search for more papers by this authorAbstract
Background
Fibrosing alveolitis is characterized by inflammation, fibrosis and increased numbers of activated CD4+ T-cells in the lower respiratory tract. The aims of this study were to compare the T-cell antigen receptor repertoire in the lungs of subjects with fibrosing alveolitis systemic sclerosis (FASSc) with cryptogenic fibrosing alveolitis (CFA) and normal control subjects, to determine whether FASSc is driven by a specific T-cell trigger and is determined by a T-cell driven immune response, and to assess the clonality of CD4+ and CD8+ TcR usage in subjects with FASSc.
Materials and methods
We used reverse transcription polymerase chain reaction with specific Vα- and Vβ-chain primers to identify the TcR gene usage in biopsy material, bronchoalveolar lavage fluid or peripheral blood from our subjects.
Results
We found individual-specific restriction of Vα- and Vβ-chain usage in lung biopsies from patients and control subjects. To establish whether this was due to expression bias in the CD4+ or CD8+ T-cells and was restricted to the lung, the αβ-T-cell receptor chain usage was assessed in T-cell subsets separated from the lungs of patients with fibrosing alveolitis and was compared with that of the peripheral blood. There was no consistent difference in the expression of any variable family chain among the population studied, although there was a significant difference between lung and peripheral blood lymphocyte Vβ-families in CD8+ T-cells (P = 0.0007).
Conclusion
We conclude that there is individual TcR Vα- and Vβ-expression bias in subjects with fibrosing alveolitis.
References
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