Brain · 2000 · 115 citations · 27 references
Life SciencesImmunologyPathologyAutoimmunityImmunopathologyInflammationAutoimmune Disease PathogenesisAutoimmune Disease PathologyInclusion Body MyositisT Cell ActivationT Cell BiologyT-cell Receptor GeneticsCd8 Positive T CellsInclusion Body LesionsMhc Class I MoleculesMhc RestrictionMuscle Fiber InvasionSkeletal MyopathyT Cell-mediated PathologyT-cell Receptor Gene Expression
Inclusion body myositis (IBM) is an inflammatory myopathy characterized immunohistologically by prominent invasion of the non-necrotic, MHC-I class antigen-expressing muscle fibres by CD8+ cytotoxic T cells. If the autoinvasive CD8+ T cells are recruited specifically to the muscle and play a primary pathogenetic role in the disease, a clonal restriction persisting over time should be anticipated. In this study, we analysed the T-cell receptor (TCR) gene usage by endomysial T lymphocytes in three sequential muscle biopsies from three different IBM patients over a 19-22 month period using immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and sequence analysis of the complementarity determining region (CDR3) of the amplified TCRs. We found that CD8+ T lymphocytes persist in the endomysial infiltrates in all biopsies during a 19-22 month period. The most frequently detected TCRs were the V beta 3, V beta 5.1, V beta 6.7 and V beta 13 gene families, and several of the autoinvasive CD8+ T cells expressed the TCRs V beta 6.7 and V beta 5.1. A restricted usage of the examined V beta 6 gene family was found to persist in the complementarity CDR3 determining region of the autoinvasive T cells over the 22 month period. Identical V beta 6 CDR3 gene arrangements were also found in the multiple muscle biopsies from two of the three IBM patients. The results indicate that in IBM there is a restricted expression of the TCR gene families among the autoinvasive T lymphocytes with homologies in the CDR3 region that persist over the course of the disease. A continuous, antigen-driven T-cell response is prominent in the muscle of patients with IBM.
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Kiichi Arahata, Andrew G. Engel · Annals of Neurology · 1984 · 632 citations
Medicine, Immunology, Pathology +13
Mark D. Howell, Jocelyn P. Diveley, Katherine A. Lundeen et al. · Proceedings of the National Academy of Sciences · 1991 · 294 citations