期刊
NATURE IMMUNOLOGY
卷 5, 期 8, 页码 809-817出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1098
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资金
- NIAID NIH HHS [AI46653, AI42767, AO50073, T32AI07485] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007337] Funding Source: Medline
Pathogen-specific CD8(+) T cells expand in number after infection and then their numbers invariably contract by 90-95%, leaving a stable memory cell pool. The chief features of this response are programmed early after infection; however, the factors regulating contraction are mostly undefined. Here we show that antibiotic treatment before Listeria monocytogenes infection induced numbers of protective memory CD8(+) T cells similar to those in control infected mice, by a pathway without contraction. The absence of contraction correlated with decreased early inflammation and interferon-gamma production and an increased fraction of CD8(+) T cells expressing the interleukin 7 receptor at the peak of the response. Thus, contraction is controlled by early inflammation but is not essential for the generation of protective memory CD8(+) T cells after infection.
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