Conclusion
Activation of T cell may be accomplished following the interaction of the TCR-CD3 complex with antigen and MHC products. In vitro this may be replaced by antibodies to the TcR or CD3 complex which mimic ligand binding. So called “alternative pathways” may also trigger activation. Activational state may be measured by lymphokine production, proliferative capacity or by expression of activation antigens. By these criteria a proportion of T cells isolated from rheumatoid joints appear to have undergone an in vivo activation. Phenotypic analysis of the synovial T cells has also established that there is an unusual distribution of Tγδ and Tαβ cells and T cell subsets in many rheumatoid patients. As T cells play a central role in immunoregulation, further exploitation of these observations using T cell clones and molecular techniques will extend our understanding of the disease process. In particular, further knowledge is required on the possible role of Tγδ cells in RA, the clonality of the T cells, the possible use of “alternative” activation pathways, and ultimately, the specificity of these T cells.
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Quayle, A., Kjeldsen-Kragh, J., Førre, Ø. et al. Immunoregulatory T cell subsets and T cell activation in rheumatoid arthritis. Springer Semin Immunopathol 11, 273–287 (1989). https://doi.org/10.1007/BF00197307
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DOI: https://doi.org/10.1007/BF00197307