Strength and elasticity of spider thread
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ID: 295561
1907
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Abstract
The chronic persistence of rheumatoid synovitis, an inflammation driven by activated T cells, macrophages, and fibroblasts causing irreversible joint damage, suggests a failure in physiologic mechanisms that down-regulate and terminate chronic immune responses. In vitro CD8+CD28−CD56+ T cells tolerize APCs, prevent the priming of naive CD4+ T cells, and suppress memory CD4+ T cell responses. Therefore, we generated CD8+CD28−CD56+ T cell clones from synovial tissues, expanded them in vitro, and adoptively transferred them into NOD-SCID mice engrafted with synovial tissues from patients with rheumatoid arthritis. Adoptively transferred CD8+CD28−CD56+ T cells displayed strong anti-inflammatory activity. They inhibited production of IFN-γ, TNF-α, and chemokines in autologous and HLA class I-matched heterologous synovitis. Down-regulation of costimulatory ligands CD80 and CD86 on synovial fibroblasts was identified as one mechanism of immunosuppression. We propose that rheumatoid synovitis can be suppressed by cell-based immunotherapy with immunoregulatory CD8+ T cells.
| Reference Key |
openalex_W2322939998
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|---|---|
| Authors | J. Benton |
| Journal | american journal of science |
| Year | 1907 |
| DOI |
10.2475/ajs.s4-24.139.75
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| URL | |
| Keywords | Keywords not found |
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