期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 7, 页码 4262-4266出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.7.4262
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资金
- NIAID NIH HHS [AI 43620] Funding Source: Medline
Recent studies suggest that the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) plays a critical role in the maintenance of self-tolerance. Using T cell-specific PTEN knockout mice (PTEN Delta T), we have identified a novel mechanism by which PTEN regulates T cell tolerance. We found that TCR stimulation alone, without CD28 costimulation, is sufficient to induce hyperactivation of the PI3K pathway, which leads to enhanced IL-2 production by naive PTEN Delta T T cells. Importantly, as a result of this increased response to TCR stimulation, PTEN Delta T CD4(+) Tcells no longer require CD28 costimulation for in vitro or in vivo expansion. In fact, unlike wild-type T cells, PTEN Delta T CD4(+) T cells are not anergized by delivery of TCR stimulation alone. These data suggest that by negatively regulating TCR signals, PTEN imposes a requirement for CD28 costimulation, thus defining a novel mechanism for its role in self-tolerance.
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