T cell regulation as a side effect of homeostasis and competition.
T cell regulation as a side effect of homeostasis and competition.
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DOI：
10.1084/jem.20021387
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发表时间：
2003-02-17
期刊：
影响因子：
--
通讯作者：
Stockinger B
中科院分区：
文献类型：
--
作者：
Barthlott T;Kassiotis G;Stockinger B
我们之前假设，维持平衡的外周免疫系统可能不是专门负责免疫调节的 T 细胞亚群的唯一责任，而且也是完整免疫系统内共享资源正常竞争的副作用。在这里，我们表明调节活动与高稳态扩张潜力相关，反映了对自肽：MHC 复合物的亲和力。具有高稳态扩张潜力且缺乏先前与调节功能相关的特征的单克隆转基因T细胞能够调节将少量初始CD45RBhi CD4 T细胞转移到淋巴细胞减少宿主中诱导的消耗性疾病。在耗尽 CD25+ T 细胞的初始多克隆 T 细胞库中也发现了自我调节功能。能够预防免疫病理的 T 细胞，如转基因 T 细胞，表达高于平均水平的 CD5，这是对自身：MHC 肽复合物的亲和力指标。因此，我们建议，无论其特异性如何，幼稚 T 细胞库的成员都可以防止淋巴细胞减少环境中潜在致病性 T 细胞的失调扩张，这是它们对稳态和抗原刺激反应的副作用。
We have previously hypothesized that maintaining a balanced peripheral immune system may not be the sole responsibility of a specialized subset of T cells dedicated to immune regulation, but also a side effect of normal competition for shared resources within an intact immune system. Here we show that regulatory activity is correlated with high homeostatic expansion potential, reflecting the avidity for self-peptide:MHC complexes. Monoclonal transgenic T cells with high homeostatic expansion potential and lacking characteristics previously associated with regulatory function were able to regulate wasting disease induced by transfer of a small number of naive CD45RBhi CD4 T cells into lymphopenic hosts. Self-regulatory function is also found in the naive polyclonal T cell repertoire depleted of CD25+ T cells. T cells capable of preventing immune pathology, like the transgenic T cells, express higher than average levels of CD5, an indicator of avidity for self:MHC peptide complexes. We therefore propose that dysregulated expansion of potentially pathogenic T cells in a lymphopenic environment can be prevented by members of the naive T cell repertoire, irrespective of their specificity, as a side effect of their response to homeostatic and antigenic stimulation.
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DOI：
10.1016/s0167-5699(99)01510-8
发表时间：
1999-10-01
期刊：
IMMUNOLOGY TODAY
影响因子：
--
作者：
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通讯作者：
Powrie, F
DOI：
10.1084/jem.188.10.1849
发表时间：
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期刊：
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影响因子：
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通讯作者：
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DOI：
10.1073/pnas.151174198
发表时间：
2001-07-31
影响因子：
11.1
作者：
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通讯作者：
Hasenkrug, KJ
影响因子：
30.5
作者：
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通讯作者：
von Boehmer, H
DOI：
10.1073/pnas.96.23.13306
发表时间：
1999-11-09
影响因子：
11.1
作者：
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通讯作者：
Jameson, SC