Journal
CANCER RESEARCH
Volume 69, Issue 4, Pages 1578-1586Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-08-2744
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Funding
- Nankai University
- NSFC [30771967]
- Ministry of Science and Technology [06C26211200695]
- 863 grant [2006AA020502]
- Tianjin [07JCZDJC03300]
- Tianjin Creative grant [06ZHCXSH04800]
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Suppressor of cytokine signaling 3 (SOCS3) expression in bone marrow cells (BMC) was up-regulated upon exposure to interleukin 6, lipopolysaccharide, or tumor-associated factors. But, how the up-regulated SOCS3 affects differentiation of BMCs is incompletely characterized. Here, we showed that SOCS3 promoted BMCs to intently differentiate into CD8 T cells. Importantly, lung can be as one athymus tissue for the BMCs to differentiate into CD8(+) T cells. Notch I plays a critical role in the differentiation from SOCS3-transfected BMCs to CD8(+) T cells. We conclude that the up-regulated SOCS3 in some pathologic conditions, such as tumor and inflammation, might promote BMCs to differentiate into CD8(+) T lymphocytes in lung tissue via up-regulating Notch1 expression. This may represent a new mechanism against diseases such as tumor. [Cancer Res 2009;69(4):1578-86]
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