Modulation of the dendritic cell-T-cell synapse to promote pathogen immunity and prevent autoimmunity
Modulation of the dendritic cell-T-cell synapse to promote pathogen immunity and prevent autoimmunity
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DOI：
10.2217/imt.11.38
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发表时间：
2011-04-01
期刊：
影响因子：
2.8
通讯作者：
Kalergis, Alexis M.
中科院分区：
文献类型：
--
作者：
Carreno, Leandro J.;Gonzalez, Pablo A.;Kalergis, Alexis M.
树突状细胞（dc）和T细胞之间的分子相互作用在对感染因子的免疫监视以及自身免疫发病机制中起着重要作用。因此，调节这种相互作用成为预防和治疗免疫紊乱以及在不引起有害炎症的情况下提高对病原体的保护的重要工具。确定DC - T细胞相互作用结果的一些分子相互作用包括：T细胞受体（TCR）与DC表面的pMHC结合，这负责抗原特异性；以及DC和T细胞表面激活/抑制受体对的比值，它们分别调节DC免疫原性和T细胞功能。这些分子正常功能的改变可能导致DC t细胞突触不平衡，从而导致无法控制感染或加剧炎症。此外，一些病原体已经发展出分子策略来破坏突触的功能以逃避适应性免疫。在这篇文章中，我们将讨论最近与DC t细胞突触控制的分子机制相关的工作，以及它们在控制自身免疫和增强病原体免疫的免疫调节中的意义。
The molecular interactions occurring at the interface between dendritic cells (DCs) and T cells play an important role in the immune surveillance against infectious agents, as well as in autoimmune pathogenesis. Therefore, regulation of this interaction arises as an important tool for the prevention and treatment of immune disorders and to improve the protection against pathogens without causing detrimental inflammation. Some of the molecular interactions defining the outcome of the DC T cell interaction are: T-cell receptor (TCR) binding to the pMHC on the DC surface, which is responsible for the antigenic specificity; and the ratio of activating/inhibitory receptor pairs on the surface of DCs and T cells, which modulate DC immunogenicity and T-cell function, respectively. An alteration in the proper function of these molecules could lead to unbalanced DC T-cell synapses that either cause a failure to control infections or exacerbated inflammation. Furthermore, some pathogens have developed molecular strategies to impair the function of the synapse to evade adaptive immunity. In this article, we will discuss recent work relative to the molecular mechanisms controlling DC T-cell synapse and their implications on immunoregulation to control autoimmunity and potentiate pathogen immunity.