细胞毒性T细胞
CD28
CD8型
白细胞介素2受体
生物
T细胞
细胞生物学
效应器
白细胞介素21
化学
免疫学
免疫系统
生物化学
体外
作者
Jinqi Liu,Clint S. Schmidt,Feisha Zhao,Angela J. Okragly,Andrew L. Glasebrook,Niles Fox,Elizabeth J. Galbreath,Qing Zhang,Ho Yeong Song,Songqing Na,Derek Yang
标识
DOI:10.1093/intimm/dxg082
摘要
LIGHT, a newly identified member of the tumor necrosis factor (TNF) family, is expressed on activated T lymphocytes. To evaluate how LIGHT contributes to T cell functions, we generated LIGHT-deficient (LIGHT(-/-)) mice using gene targeting. Disruption of LIGHT significantly reduced CD8(+) T cell-cycle progression, leading to reduced proliferation to anti-CD3, anti-CD3/anti-CD28 or allogeneic stimulation, whereas proliferation of CD4(+) T cells remained unchanged. In contrast to the observed proliferative defects, isolated CD8(+) T cells from LIGHT(-/-) mice displayed normal cytotoxic effector function development when compared to wild-type CD8(+) T cells. Underlying a potential mechanism of reduced CD8(+) T cell proliferation, LIGHT(-/-) CD8(+) T cells displayed reduced surface levels of CD25 and a diminished ability to proliferate in response to exogenous IL-2. Furthermore, addition of IL-12 to LIGHT(-/-) CD8(+) T cell cultures could not ameliorate this proliferative defect. These results reveal a potential mechanism of action for LIGHT as a positive regulator of CD8(+) T cell expansion, but not lytic effector function development.
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