Abstract
Recent studies by Chatenoud and co-workers suggest that non-mitogenic F(ab′)2 fragments of anti-CD3 antibodies, which cannot bind the Fc receptor, induce a prolonged period of tolerance and prevent diabetes in nonobese diabetic (NOD) mice. Tolerance is established by regulatory T cells through the production of transforming growth factor-β1 (TGF-β1), but the mechanism by which TGF-β1 confers this activity is unclear. Analysis of mice deficient in TGF-β1 suggests that TGF-β1 raises the threshold at which intracellular calcium activates T cells to a level that prevents an autoimmune response.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3-9 |
| Number of pages | 7 |
| Journal | Trends in Molecular Medicine |
| Volume | 10 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2004 |
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology
Fingerprint
Dive into the research topics of 'TGF-β, T-cell tolerance and anti-CD3 therapy'. Together they form a unique fingerprint.Cite this
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS