TIM-4, a receptor for phosphatidylserine, controls adaptive immunity by regulating the removal of antigen-specific T cells.
TIM-4, a receptor for phosphatidylserine, controls adaptive immunity by regulating the removal of antigen-specific T cells.
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TIM-4是一种磷脂酰丝氨酸的受体,通过调节去除抗原特异性T细胞来控制适应性免疫。
DOI:
10.4049/jimmunol.1001360
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发表时间:
2010-12-01
期刊:
影响因子:
--
通讯作者:
DeKruyff RH
中科院分区:
文献类型:
--
作者:
Albacker LA;Karisola P;Chang YJ;Umetsu SE;Zhou M;Akbari O;Kobayashi N;Baumgarth N;Freeman GJ;Umetsu DT;DeKruyff RH
Adaptive immunity is characterized by the expansion of an Ag-specific T cell population following Ag exposure. The precise mechanisms, however, that control the expansion and subsequent contraction in the number of Ag-specific T cells are not fully understood. We show that T cell/transmembrane, Ig, and mucin (TIM)-4, a receptor for phosphatidylserine, a marker of apoptotic cells, regulates adaptive immunity in part by mediating the removal of Ag-specific T cells during the contraction phase of the response. During Ag immunization or during infection with influenza A virus, blockade of TIM-4 on APCs increased the expansion of Ag-specific T cells, resulting in an increase in secondary immune responses. Conversely, overexpression of TIM-4 on APCs in transgenic mice reduced the number of Ag-specific T cells that remained after immunization, resulting in reduced secondary T cell responses. There was no change in the total number of cell divisions that T cells completed, no change in the per cell proliferative capacity of the remaining Ag-specific T cells, and no increase in the development of Ag-specific regulatory T cells in TIM-4 transgenic mice. Thus, TIM-4–expressing cells regulate adaptive immunity by mediating the removal of phosphatidylserine-expressing apoptotic, Ag-specific T cells, thereby controlling the number of Ag-specific T cells that remain after the clearance of Ag or infection.
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影响因子:
64.5
作者:
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通讯作者:
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影响因子:
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DOI:
10.1073/pnas.0538056100
发表时间:
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影响因子:
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