| First Author | Maksimow M | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 79 |
| Issue | 2 | Pages | 369-77 |
| PubMed ID | 16330535 | Mgi Jnum | J:105877 |
| Mgi Id | MGI:3616923 | Doi | 10.1189/jlb.0505238 |
| Citation | Maksimow M, et al. (2006) Fas costimulation of naive CD4 T cells is controlled by NF-kappaB signaling and caspase activity. J Leukoc Biol 79(2):369-77 |
| abstractText | Fas ligation induces apoptosis of activated T cells via the caspase cascade but can also mediate costimulatory signals to naive T cells at the time of activation. We have previously shown that Fas ligation of naive CD4 T cells activated by dendritic cells induces death or accelerates their proliferation and increases interferon-gamma (IFN-gamma) production. To understand this costimulation, we investigated the roles of caspases and nuclear factor (NF)-kappaB in survival and proliferation of responding T cells. Fas ligation increased caspase-3 and -8 activities during T cell activation, irrespective of cell fate. The accelerated proliferation induced by Fas ligation could be reduced by selective inhibition of both caspases. Inhibition of NF-kappaB simultaneously with Fas ligation inhibited the increased IFN-gamma production and caused uniform death of all responding T cells. Thus, Fas-mediated costimulation of naive CD4 T cells is driven by active caspases, and NF-kappaB acts as a dominant survival-supporting factor of Fas-costimulated cells containing high levels of activated caspase-8 and -3. |
