Regulatory T cells in infection.

Regulatory T cells in infection.
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DOI:
10.1016/b978-0-12-387827-4.00003-6
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发表时间:
2011
影响因子:
--
通讯作者:
Smith KA
Smith KA
中科院分区:
医学3区
文献类型:
--
作者:
Maizels RM;Smith KA

文献摘要

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感染性病原体与宿主免疫系统密切协同进化,获得了一系列高度复杂的机制来调节免疫。在病毒、细菌、原生动物、蠕虫和真菌开发的常见策略中,操纵调节性T细胞网络以利于病原体的生存和传播。在许多情况下,Treg活性还通过控制对感染的免疫病理反应而有益于宿主。有趣的是,一些病原体能够直接诱导原始T细胞转化为抑制Foxp3表达的Tregs,而另一些病原体能够激活原有的自然Tregs,在这两种情况下都能抑制病原体特异性的效应器反应。然而,在某些情况下,Treg也可以促进免疫,例如在感染的初始阶段,效应器细胞必须进入感染部位,随后在确保效应器记忆的产生方面。值得注意的是,目前几乎没有关于感染是否选择性地驱动病原体特异性Tregs的信息,如果是的话,这些细胞是否也对自身抗原起反应。对特异性的进一步分析,以及对Treg亚群在病程中的相对动态的更清晰的描述,应该会导致免疫干预的合理策略,以优化免疫和消除感染。
Infectious agents have intimately co-evolved with the host immune system, acquiring a portfolio of highly sophisticated mechanisms to modulate immunity. Among the common strategies developed by viruses, bacteria, protozoa, helminths, and fungi is the manipulation of the regulatory T cell network in order to favor pathogen survival and transmission. Treg activity also benefits the host in many circumstances by controlling immunopathogenic reactions to infection. Interestingly, some pathogens are able to directly induce the conversion of naive T cells into suppressive Foxp3-expressing Tregs, while others activate pre-existing natural Tregs, in both cases repressing pathogen-specific effector responses. However, Tregs can also act to promote immunity in certain settings, such as in initial stages of infection when effector cells must access the site of infection, and subsequently in ensuring generation of effector memory. Notably, there is little current information on whether infections selectively drive pathogen-specific Tregs, and if so whether these cells are also reactive to self-antigens. Further analysis of specificity, together with a clearer picture of the relative dynamics of Treg subsets over the course of disease, should lead to rational strategies for immune intervention to optimize immunity and eliminate infection.