The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Inhibition of T cell apoptosis in the rheumatoid synovium.
Open accessAbstract
Synovial T cells in rheumatoid arthritis are highly differentiated and express a phenotype suggesting susceptibility to apoptosis (CD45RB dull, CD45RO bright, Bcl-2 low, Bax high, Fas high). However, no evidence of T cell apoptosis was found in synovial fluid from any of 28 patients studied. In contrast, synovial fluid from 10 patients with crystal arthritis showed substantial levels of T cell apoptosis. The failre of apoptosis was not an intrinsic property of rheumatoid synovial T cells, as they showed rapid spontaneous apoptosis on removal from the joint. Synovial T cells from rheumatoid arthritis and gout patients could be rescued from spontaneous apoptosis in vitro either by IL-2R gamma chain signaling cytokines (which upregulate Bcl-2 and Bcl-XL) or by interaction with synovial fibroblasts (which upregulates Bcl-xL but not Bcl-2). The phenotype of rheumatoid synovial T cells ex vivo (Bcl-2 low, Bcl-xL high) suggested a fibroblast-mediated mechanism in vivo. This was confirmed by in vitro culture of synovial T cells with fibroblasts which maintained the Bcl-xL high Bcl-2 low phenotype. Synovial T cells from gout patients were Bcl-2 low Bcl-xL low and showed clear evidence of apoptosis in vivo. Inhibition experiments suggested that an integrin-ligand interaction incorporating the Arg-Gly-Asp motif is involved in fibroblast-mediated synovial T cell survival. We propose that environmental blockade of cell death resulting from interaction with stromal cells is a major factor in the persistent T cell infiltration of chronically inflamed rheumatoid synovium.
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Arnett, F. C., Edworthy, S. M., Bloch, D. A., Mcshane, D. J., Fries, J. F., Cooper, N. S., Healey, L. A., Kaplan, S. R., Liang, M. H., Luthra, H. S., et al. (1988) · Arthritis & Rheumatism · doi:10.1002/art.1780310302 · Cited by 19,752
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
Oltval, Z. N., Milliman, C. L., & Korsmeyer, S. J. (1993) · Cell · doi:10.1016/0092-8674(93)90509-o · Cited by 6,003
Vermes, I., Haanen, C., Steffens-Nakken, H., & Reutellingsperger, C. (1995) · Journal of Immunological Methods · doi:10.1016/0022-1759(95)00072-i · Cited by 5,410
bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death
Boise, L. H., González-García, M., Postema, C. E., Ding, L., Lindsten, T., Turka, L. A., Mao, X., Nuñez, G., & Thompson, C. B. (1993) · Cell · doi:10.1016/0092-8674(93)90508-n · Cited by 3,087
Martin, S. J., Reutelingsperger, C. P., McGahon, A. J., Rader, J. A., van Schie, R. C., LaFace, D. M., & Green, D. R. (1995) · The Journal of experimental medicine · doi:10.1084/jem.182.5.1545 · Cited by 2,824
Autocrine T-cell suicide mediated by APO-1/(Fas/CD95)
Dhein, J., Walczak, H., Bäumler, C., Debatin, K.-M., & Krammer, P. H. (1995) · Nature · doi:10.1038/373438a0 · Cited by 1,609
Programmed Cell Death and the Control of Cell Survival: Lessons from the Nervous System
Raff, M. C., Barres, B. A., Burne, J. F., Coles, H. S., Ishizaki, Y., & Jacobson, M. D. (1993) · Science · doi:10.1126/science.8235590 · Cited by 1,460
Cloning of a T Cell Growth Factor that Interacts with the β Chain of the Interleukin-2 Receptor
Grabstein, K. H., Eisenman, J., Shanebeck, K., Rauch, C., Srinivasan, S., Fung, V., Beers, C., Richardson, J., Schoenborn, M. A., Ahdieh, M., et al. (1994) · Science · doi:10.1126/science.8178155 · Cited by 1,422
Brunner, T., Mogil, R. J., LaFace, D., Yoo, N. J., Mahboubi, A., Echeverri, F., Martin, S. J., Force, W. R., Lynch, D. H., Ware, C. F., et al. (1995) · Nature · doi:10.1038/373441a0 · Cited by 1,314
Smith, C. A., Williams, G. T., Kingston, R., Jenkinson, E. J., & Owen, J. J. T. (1989) · Nature · doi:10.1038/337181a0 · Cited by 1,133
Cited by
Anti-TNFα Therapy of Rheumatoid Arthritis: What Have We Learned?
Feldmann, M., & Maini, R. N. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.163 · Cited by 1,257
Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation
Buckley, C. D., Pilling, D., Lord, J. M., Akbar, A. N., Scheel-Toellner, D., & Salmon, M. (2001) · Trends in Immunology · doi:10.1016/s1471-4906(01)01863-4 · Cited by 796
Self-citationDirecting Transition from Innate to Acquired Immunity: Defining a Role for IL-6
Jones, S. A. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.175.6.3463 · Cited by 771
Pilling, D., Fan, T., Huang, D., Kaul, B., & Gomer, R. H. (2009) · PLoS ONE · doi:10.1371/journal.pone.0007475 · Cited by 433
Self-citationPivotal Advance: Th-1 cytokines inhibit, and Th-2 cytokines promote fibrocyte differentiation
Shao, D. D., Suresh, R., Vakil, V., Gomer, R. H., & Pilling, D. (2008) · Journal of Leukocyte Biology · doi:10.1189/jlb.1107782 · Cited by 272
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Metadata
- Authors
- Salmon, M., Scheel-Toellner, D., Huissoon, A. P., Pilling, D., Shamsadeen, N., Hyde, H., D'Angeac, A. D., Bacon, P. A., Emery, P., & Akbar, A. N.
- Venue
- Journal of Clinical Investigation
- Published
- 1997-02-01
- Volume
- 99
- Issue
- 3
- Pages
- 439-446
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2064976851
- Cited by
- 469
- References
- 36
- FWCI
- 14.13
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Salmon, M., Scheel-Toellner, D., Huissoon, A. P., Pilling, D., Shamsadeen, N., Hyde, H., D'Angeac, A. D., Bacon, P. A., Emery, P., & Akbar, A. N. (1997). Inhibition of T cell apoptosis in the rheumatoid synovium. Journal of Clinical Investigation. https://doi.org/10.1172/jci119178
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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