期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 195, 期 12, 页码 1533-1539出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20020067
关键词
T lymphocytes; homeostasis; cytokines; mice; transgenic
资金
- NCI NIH HHS [CA38355, R37 CA038355] Funding Source: Medline
- NHLBI NIH HHS [HL07196] Funding Source: Medline
- NIAID NIH HHS [AI41079, R01 AI045809, R01 AI046710, T32 AI007244, AI07244, AI45809, AI21487, AI46710] Funding Source: Medline
- NIA NIH HHS [R01 AG020186, AG20186] Funding Source: Medline
Transgenic (TG) mice expressing a high copy number of interleukin (IL)-7 cDNA under the control of the major histocomaptability complex (MHC) class 11 promoter display a 10-20-fold increase in total T cell numbers, Here, we show, that the increase in T cell numbers in IL-7 TG mice is most apparent at the level of memory phenotype CD44(bi) CD 122(bi) CD8(+) cells. Based on studies with T cell receptor (TCR) TG mice crossed to IL-7 TG mice, increased levels of IL-7 may provide costimulation for TCR recognition of self-MHC ligands and thus Cause naive CD8(+) cells to proliferate and differentiate into memory phenotype cells. In addition, a marked increase in CD44(bi) CD122(bi) CD8(+) cells was found in IL-7 TG IL-15(-) mice. Since these cell are rare in normal IL-15(-) mice, the dependency of memory phenotype CD8(+), cells on IL-15 can be overcome by overexpression of IL-7.
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