Following an acute T cell response, most activated effector cells die, while some survive and become memory cells. The pro-apoptosic Bcl-2 family member, Bcl-2 interacting mediator of death (Bim) is critical for eliminating most effector T cells, while expression of CD127 (IL-7Rα) 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 CD127lo LCMV-specific CD4+ and CD8+ T cells were lost in wild-type mice, but were spared in Bim-/- mice. Further, while the numbers of CD127hi 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 CD127lo 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. © 2006 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
