| First Author | Cannons JL | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 6 | Pages | 2828-31 |
| PubMed ID | 12218092 | Mgi Jnum | J:78961 |
| Mgi Id | MGI:2386527 | Doi | 10.4049/jimmunol.169.6.2828 |
| Citation | Cannons JL, et al. (2002) Cutting Edge: Profound Defect in T Cell Responses in TNF Receptor-Associated Factor 2 Dominant Negative Mice. J Immunol 169(6):2828-31 |
| abstractText | TNFR-associated factor 2 (TRAF2) is an adapter protein that links several members of the TNFR family to downstream signaling pathways. Mice expressing a dominant negative form of TRAF2 in their lymphoid cells (TRAF2.DN mice) have a profound defect in T cell responses to allogeneic APC. In contrast, APC from wild-type or TRAF2.DN mice show an equivalent level of stimulation in a MLR. Ab production and class switch are unimpaired in TRAF2.DN mice. Thus, defects in the TRAF.DN mice appear to be limited to T cells. TRAF2.DN mice demonstrate an impaired T cell response to influenza virus, including decreased secondary expansion of IFN-gamma-secreting T cells as well as a decrease in CTL activity. CD4 T cell production of IL-2 was also dramatically impaired in TRAF2.DN mice. These studies suggest an essential role of TRAF2-linked receptors in secondary CD4 and CD8 T cell responses and have important implications for transplantation. |
