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Acquisition of regulatory function by human CD8(+) T cells treated with anti-CD3 antibody requires TNF.

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.

journal_name

Eur J Immunol

journal_title

European journal of immunology

authors

Ablamunits V,Bisikirska B,Herold KC

doi

10.1002/eji.201040485

subject

Has Abstract

pub_date

2010-10-01 00:00:00

pages

2891-901

issue

10

eissn

0014-2980

issn

1521-4141

journal_volume

40

pub_type

杂志文章

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