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- W2014553274 abstract "Abstract Anti‐CD3 mAb can modulate graft rejection and attenuate autoimmune diseases but their mechanism(s) of action remain unclear. CD8 + T cells with regulatory function are induced in vitro by Teplizumab, a humanized anti‐CD3 antibody and inhibit responses of autologous and allogeneic T cells. They inhibit CD4 + T‐cell proliferation by mechanisms involving TNF and CCL4, and by blocking target cell entry into G2/M phase of cell cycle but neither kill them, nor compete for IL‐2. CD8 + Treg can be isolated from peripheral blood following treatment of patients with Type 1 diabetes with Teplizumab, but not from untreated patients. The induction of CD8 + Treg by anti‐CD3 mAb requires TNF and signaling through the NF‐κB cascade. The CD8 + Treg express CD25, glucocorticoid‐induced TNF receptor family, CTLA‐4, Foxp3, and TNFR2, and the combined expression of TNFR2 and CD25 identifies a potent subpopulation of CD8 + Treg. These studies have identified a novel mechanism of immune regulation by anti‐CD3 mAb and markers that may be used to track inducible CD8 + Treg in settings such as chronic inflammation or immune therapy." @default.
- W2014553274 created "2016-06-24" @default.
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- W2014553274 date "2010-07-20" @default.
- W2014553274 modified "2023-10-18" @default.
- W2014553274 title "Acquisition of regulatory function by human CD8+ T cells treated with anti-CD3 antibody requires TNF" @default.
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- W2014553274 doi "https://doi.org/10.1002/eji.201040485" @default.
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