| First Author | Zeng H | Year | 2008 |
| Journal | J Biol Chem | Volume | 283 |
| Issue | 36 | Pages | 24392-9 |
| PubMed ID | 18583339 | Mgi Jnum | J:141752 |
| Mgi Id | MGI:3819702 | Doi | 10.1074/jbc.M802344200 |
| Citation | Zeng H, et al. (2008) T cell receptor-mediated activation of CD4+CD44hi T cells bypasses Bcl10: an implication of differential NF-kappaB dependence of naive and memory T cells during T cell receptor-mediated responses. J Biol Chem 283(36):24392-9 |
| abstractText | Previous studies have demonstrated that Bcl10 (B-cell leukemia/lymphoma 10) is essential for T cell receptor-mediated NF-kappaB activation and subsequent proliferation and interleukin 2 (IL2) production. However, here we demonstrate that, contrary to expectations, Bcl10 is differentially required for T cell activation, including for both proliferation and cytokine production. When CD4+ and CD8+ T cells were divided based on expression levels of CD44, which distinguishes naive cells (CD44lo) versus those that are antigen-experienced (CD44hi), IL2 production by and proliferation of CD4+CD44lo naive cells and both subpopulations of CD8+ T cells were clearly Bcl10-dependent, whereas these same functional properties of CD4+CD44hi T cells occurred largely independent of Bcl10. As with the other subpopulations of T cells, CD4+CD44hi T cells did not activate the NF-kappaB pathway in the absence of Bcl10; nevertheless, these CD4+CD44hi antigen-experienced T cells efficiently secreted IL2 after T cell receptor stimulation. Strikingly, therefore, T cell receptor-mediated IL2 production in these cells is NF-kappaB-independent. Our studies suggest that antigen-experienced CD4+ T cells differ from their naive counterparts and from CD8+ T cells in their ability to achieve activation independent of the Bcl10/NF-kappaB pathway. |
