Boasso Adriano, Vaccari Monica, Nilsson Jakob, Shearer Gene M, Andersson Jan, Cecchinato Valentina, Chougnet Claire, Franchini Genoveffa
Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892, USA
AIDS Rev. 2006 Jul-Sep;8(3):141-7.
The impairment of adaptive immune responses to HIV and abnormalities in the immune regulatory function mechanisms during HIV infection have been regarded as key issues in AIDS pathogenesis since the early years of the pandemic. However, the multiple mechanisms underlying this impairment are still not fully understood. New emerging information shows that alterations in the number and/or function of regulatory T-cells may contribute to HIV pathogenesis. Thus, pharmacologic manipulation of regulatory T-cells as well as blocking the activity of other immunomodulatory molecules, such as indoleamine 2,3-dioxygenase, glucocorticoid-induced tumor necrosis factor receptor and PD1, might provide a valuable approach to redirect the immune system towards an efficient antiviral response.
自艾滋病流行早期以来，HIV感染过程中适应性免疫反应的损害以及免疫调节功能机制的异常就被视为艾滋病发病机制的关键问题。然而，这种损害背后的多种机制仍未完全被理解。新出现的信息表明，调节性T细胞数量和/或功能的改变可能有助于HIV发病机制。因此，对调节性T细胞进行药物调控以及阻断其他免疫调节分子的活性，如吲哚胺2,3-双加氧酶、糖皮质激素诱导的肿瘤坏死因子受体和程序性死亡受体1，可能为使免疫系统转向有效的抗病毒反应提供一种有价值的方法。
