| First Author | Arechiga AF | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 12 | Pages | 7800-4 |
| PubMed ID | 16339514 | Mgi Jnum | J:122653 |
| Mgi Id | MGI:3714958 | Doi | 10.4049/jimmunol.175.12.7800 |
| Citation | Arechiga AF, et al. (2005) Cutting edge: FADD is not required for antigen receptor-mediated NF-kappaB activation. J Immunol 175(12):7800-4 |
| abstractText | Recently, it has been demonstrated that stimulated T cells bearing defects in caspase-8 fail to promote nuclear shuttling of NF-kappaB complexes. Such cells display strikingly similar proliferative and survival defects as T cells lacking Fas-associated death domain protein (FADD) function. We characterized NF-kappaB signaling in T cells bearing a dominant-negative FADD transgene (FADDdd). Whereas FADDdd T cells displayed proliferative defects following activation, these were not a consequence of aberrant NF-kappaB signaling, as measured by IKK/IkappaB phosphorylation and IkappaB degradation. There were no appreciable defects in nuclear translocation of p65/Rel using ImageStream, a flow-based imaging cytometer. Pretreatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, a potent caspase inhibitor, also failed to impede canonical NF-kappaB signaling. Secretion of IL-2 and up-regulation of various activation markers occurred normally. Thus, FADD does not play an essential role in NF-kappaB activation, suggesting an alternative route by which this adaptor promotes the clonal expansion of T cells. |
