| First Author | Sun J | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 7 | Pages | 4783-8 |
| PubMed ID | 16177127 | Mgi Jnum | J:118958 |
| Mgi Id | MGI:3700869 | Doi | 10.4049/jimmunol.175.7.4783 |
| Citation | Sun J, et al. (2005) Essential roles of the Fas-associated death domain in autoimmune encephalomyelitis. J Immunol 175(7):4783-8 |
| abstractText | The Fas-associated death domain (FADD) protein mediates apoptosis by coupling death receptors with the caspase cascade. Paradoxically, it also promotes cell mitosis through its C-terminal region. Apoptosis and mitosis are opposing processes that can have radically different consequences. To determine which of the FADD effects prevails in T cell-mediated autoimmune diseases, we studied myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) using mice that express a dominant-negative FADD (FADD-DN) transgene in the T cell lineage. We found that FADD blockade in T cells prevented the development of autoimmune encephalomyelitis and inhibited both Th1 and Th2 type responses. Myelin oligodendrocyte glycoprotein-specific T cell proliferation was also dramatically reduced in FADD-DN mice despite the resistance of T cells to activation-induced cell death. These results indicate that although FADD expressed by T cells is involved in regulating both mitosis and apoptosis, its effect on mitosis prevails in EAE, and that strategies inhibiting FADD functions in T cells could be effective in preventing the disease. |
