| First Author | Murano M | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 79 |
| Issue | 1 | Pages | 140-6 |
| PubMed ID | 16244108 | Mgi Jnum | J:104742 |
| Mgi Id | MGI:3612734 | Doi | 10.1189/jlb.0505271 |
| Citation | Murano M, et al. (2006) Latent TGF-{beta}1-transduced CD4+ T cells suppress the progression of allergic encephalomyelitis. J Leukoc Biol 79(1):140-6 |
| abstractText | Systemic injection of small amounts of transforming growth factor-beta (TGF-beta), a cytokine produced by lymphoid and other cells, has a profound effect in protecting mice from the inflammatory demyelinating lesions of experimental allergic encephalomyelitis (EAE; an animal model for multiple sclerosis). However, TGF-beta has side-effects, which might be avoided if the cells producing TGF-beta can be delivered to the affected site in the nervous system to insure its local release in small amounts. Myelin basic protein (MBP)-specific, cloned CD4(+) T cells were engineered by retroviral transduction to produce latent TGF-beta. Studies about the spontaneous form of EAE in T cell receptor (TCR)-transgenic recombination-activating gene (RAG)-1(-/-) mice showed that essentially all of the MBP-specific, TCR-transgenic RAG-1(-/-) (BALB/cxB10.PL)F1 mice develop spontaneous EAE by the age of 11 weeks. By 12 weeks, 25-50% of the mice have died from disease. A single injection of TGF-beta1-transduced T helper cell type 1 (Th1) cells significantly protected the mice from EAE, and untransduced Th1 cells did not protect. MBP-specific BALB/c Th2 clones, transduced with TGF-beta1-internal ribosome entry site-green fluorescent protein (GFP) significantly reduced EAE induction by untransduced Th1 cells in RAG-1(-/-) B10.PL mice. Furthermore, the GFP(+) TGF-beta1-producing Th2 cells were detectable in the spinal cords of the injected mice. |
