作者: Sara Wojciechowski , Pulak Tripathi , Tristan Bourdeau , Luis Acero , H. Leighton Grimes
DOI: 10.1084/JEM.20070618
关键词:
摘要: We examined the role of antiapoptotic molecule Bcl-2 in combating proapoptotic Bim control naive and memory T cell homeostasis using Bcl-2(-/-) mice that were additionally deficient one or both alleles Bim. Naive cells significantly decreased Bim(+/-)Bcl-2(-/-) mice, but largely restored Bim(-/-)Bcl-2(-/-) mice. Similarly, a synthetic inhibitor killed wild-type, not Bim(-/-), cells. Further, from died rapidly ex vivo refractory to cytokine-driven survival vitro. In vivo, CD8(+) required combat maintain peripheral survival, whereas CD4(+) did not. contrast, generated relatively normal numbers after lymphocytic choriomeningitis virus infection. Accumulation was likely caused by their increased proliferative renewal because lymphopenic environment Collectively, these data demonstrate critical for balance between controlling