| First Author | Kim EY | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 12 | Pages | 6812-20 |
| PubMed ID | 11739497 | Mgi Jnum | J:107039 |
| Mgi Id | MGI:3619944 | Doi | 10.4049/jimmunol.167.12.6812 |
| Citation | Kim EY, et al. (2001) TNF type 2 receptor (p75) lowers the threshold of T cell activation. J Immunol 167(12):6812-20 |
| abstractText | T cell activation requires a threshold amount of TCR-mediated signals, an amount that is reduced by signals mediated through costimulatory molecules expressed on the T cell surface. Here the role of TNFR2 (p75) as a putative costimulatory receptor for T cell activation was examined. It was found that p75 deficiency in CD8(+) T cells increased the requirements for TCR agonist approximately 5-fold. Furthermore, p75(-/-) T cells display a marked reduction in the proliferative response to TCR agonist. This hypoproliferative response was associated with delayed kinetics of induction of the acute activation markers CD25 and CD69 as well as a marked decrease in the production of IL-2 and IFN-gamma. The net result is that very few cells are recruited into the dividing population. Interestingly, CD28 costimulation was only partially effective in rescuing the proliferative defect of p75(-/-)CD8(+) T cells. Thus, p75 provides an important costimulatory signal in addition to that provided by CD28 toward optimal T cell proliferation. |
