A model of suppression of the antigen-specific CD4 T cell response by regulatory CD25+CD4 T cells in vivo.

A model of suppression of the antigen-specific CD4 T cell response by regulatory CD25+CD4 T cells in vivo.
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体内调节性 CD25 CD4 T 细胞抑制抗原特异性 CD4 T 细胞反应的模型。

DOI:
10.1093/intimm/dxh213
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发表时间:
2005
期刊:
International immunology.
影响因子:
--
通讯作者:
Khoruts,Alexander
Khoruts,Alexander
中科院分区:
--
文献类型:
--
作者:
Thorstenson,KristenM;Herzovi,Laura;Khoruts,Alexander

文献摘要

相似文献

尽管最近引起了强烈的兴趣,但调节性CD 25 + CD 4 T细胞的抑制机制仍然知之甚少。该领域的一个缺陷是缺乏体内模型,其中调节性CD 25 + CD 4 T细胞对抗原特异性应答T细胞的作用可以定量测量。我们在这里描述一个这样的模型。我们比较了同基因CD 28 −/−和野生型受体小鼠中过继转移的幼稚野生型抗原特异性CD 4 T细胞对标称抗原的反应。这些细胞在CD 28 −/−小鼠中表现出更大程度的增殖和分化,并且不能通过全身暴露于无促排剂的抗原而呈现功能性低反应。我们能够找到解释这种差异的唯一原因是CD 28 −/−小鼠中调节性CD 25 + CD 4 T细胞的缺乏。使用CD 28 −/−小鼠作为过继转移受体提供了一个简单的模型,揭示了调节性CD 25 + CD 4 T细胞在体内控制抗原驱动的应答中的作用。
Despite intense recent interest, the suppressive mechanisms of regulatory CD25+CD4 T cells remain poorly understood. One deficiency in the field is the lack ofin vivomodels where the effects of regulatory CD25+CD4 T cells on antigen-specific responder T cells can be measured quantitatively. We describe one such model here. We compared responses of adoptively transferred naive wild-type antigen-specific CD4 T cells in syngeneic CD28−/− and wild-type recipient mice toward a nominal antigen. The cells exhibited a greater degree of proliferation and differentiation in CD28−/− mice and could not be rendered functionally hyporesponsive by systemic exposure to adjuvant-free antigen. The only reason we were able to find to explain this difference was the deficiency of regulatory CD25+CD4 T cells in the CD28−/− mice. Use of CD28−/− mice as adoptive transfer recipients provides a simple model that reveals the contribution of regulatory CD25+CD4 T cells in controlling antigen-driven responsesin vivo.