El-Far Mohamed, Halwani Rabih, Said Elias, Trautmann Lydie, Doroudchi Mehrnoosh, Janbazian Loury, Fonseca Simone, van Grevenynghe Julien, Yassine-Diab Bader, Sékaly Rafick-Pierre, Haddad Elias K
Centre de Recherche du CHUM, Hôpital Saint-Luc, 264, René-Lévesque est, Bureau 1317, Montréal, Québec, H2X 1P1, Canada.
Curr HIV/AIDS Rep. 2008 Feb;5(1):13-9. doi: 10.1007/s11904-008-0003-7.
Generation of memory T cells, which mediate immunity against microbes and cancers, relies, for optimal activity, on the interactions of multiple cell types that are highly regulated through the expression of soluble factors and negative and positive receptors. Their disruption will lead to aberrant immune responses, which can result in the invasion of the host by foreign pathogens. In chronic viral infections including HIV and hepatitis C virus, persistence of antigen and lack of CD4 help (HIV) disrupt memory T-cell function and induce defects in memory T-cell responses, which have been defined as T-cell exhaustion. In this review, we examine the molecular mechanisms involved in such T-cell dysfunction. Better understanding of these mechanisms will assist in the development of novel therapies to prevent the immune damage mediated by HIV infection.
记忆T细胞介导针对微生物和癌症的免疫,其最佳活性依赖于多种细胞类型的相互作用,这些细胞类型通过可溶性因子以及阴性和阳性受体的表达受到高度调节。它们的破坏会导致异常的免疫反应,进而可能导致外来病原体入侵宿主。在包括HIV和丙型肝炎病毒在内的慢性病毒感染中,抗原的持续存在以及CD4辅助功能的缺失(HIV感染)会破坏记忆T细胞功能,并导致记忆T细胞反应出现缺陷,这被定义为T细胞耗竭。在本综述中,我们研究了此类T细胞功能障碍所涉及的分子机制。对这些机制的深入理解将有助于开发新的疗法,以预防HIV感染介导的免疫损伤。