| First Author | Wojciechowski S | Year | 2006 |
| Journal | Eur J Immunol | Volume | 36 |
| Issue | 7 | Pages | 1694-706 |
| PubMed ID | 16761315 | Mgi Jnum | J:115833 |
| Mgi Id | MGI:3692248 | Doi | 10.1002/eji.200635897 |
| Citation | Wojciechowski S, et al. (2006) Bim mediates apoptosis of CD127(lo) effector T cells and limits T cell memory. Eur J Immunol 36(7):1694-706 |
| abstractText | Following an acute T cell response, most activated effector cells die, while some survive and become memory cells. The pro-apoptotic Bcl-2 family member, Bcl-2 interacting mediator of death (Bim) is critical for eliminating most effector T cells, while expression of CD127 (IL-7Ralpha) has been proposed to mark effector cells destined to become memory cells. Here, we examined the effects of Bim on the death of effector T cells in relationship to CD127 expression and on development of T cell memory following lymphocytic choriomeningitis virus (LCMV) infection. We found that large numbers of CD127(lo) LCMV-specific CD4(+) and CD8(+) T cells were lost in wild-type mice, but were spared in Bim(-/-) mice. Further, while the numbers of CD127(hi) T cells declined only slightly during contraction of the response in wild-type mice, they increased significantly in Bim(-/-) mice due to re-expression of CD127 on CD127(lo) T cells that had avoided apoptosis. Functional memory T cells were significantly increased in Bim(-/-) mice; however, they underwent a slow attrition due to decreased proliferative renewal. Taken together, these data suggest that the absence of Bim-mediated death of LCMV-specific CD4(+) and CD8(+) T cells in vivo can increase T cell memory, but other homeostatic mechanisms control the long-term maintenance of memory cells. |
