期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 7, 页码 4247-4251出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.7.4247
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资金
- NIAID NIH HHS [AI 41576, R01 AI051583-05, R56 AI051583, F32 AI053970, AI 053970, R01 AI051583, AI 51583, R01 AI041576] Funding Source: Medline
- NIDDK NIH HHS [DK 5260] Funding Source: Medline
Expression of IL-7Ra on a subset of Ag-specific effector CD8 T cells is believed to identify memory cell precursors. However, whether IL-7 regulates IL-7R alpha expression in vivo and is responsible for selective survival of IL-7R alpha(+) effector cells is unknown. Our results show that in the absence of IL-7, IL-7R alpha expression was extinguished on the majority of CD8 T cells responding to virus infection, sustained on a subset of effector cells transitioning to memory, and expressed at high levels by memory cells. Additionally, an IL-7-deficient environment was capable of supporting bcl-2 up-regulation and memory cell development in response to virus infection. Thus, IL-7R alpha regulation occurs independently of IL-7 in responding CD8 T cells, indicating that CD8 memory T cell precursors are not selected by IL-7/IL-7R alpha interactions.
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