Ruiz-Pablos Manuel
Faculty of Medicine, European University of Madrid, 28670 Madrid, Spain.
Pathogens. 2022 Jul 25;11(8):831. doi: 10.3390/pathogens11080831.
Activated cytotoxic CD4 T cells (HLA-DR+) play an important role in the control of EBV infection, especially in cells with latency I (EBNA-1). One of the evasion mechanisms of these latency cells is generated by gp42, which, via peripherally binding to the β1 domain of the β chain of MHC class II (HLA-DQ, -DR, and -DP) of the infected B lymphocyte, can block/alter the HLA class II/T-cell receptor (TCR) interaction, and confer an increased level of susceptibility towards the development of EBV-associated autoimmune diseases or cancer in genetically predisposed individuals (HLA-DRB1* and DQB1* alleles). The main developments predisposing the factors of these diseases are: EBV infection; HLA class II risk alleles; sex; and tissue that is infiltrated with EBV-latent cells, forming ectopic lymphoid structures. Therefore, there is a need to identify treatments for eliminating cells with EBV latency, because the current treatments (e.g., antivirals and rituximab) are ineffective.
活化的细胞毒性CD4 T细胞（HLA-DR+）在控制EBV感染中起重要作用，尤其是在处于I型潜伏期（EBNA-1）的细胞中。这些潜伏期细胞的一种逃逸机制是由gp42产生的，gp42通过在外周与被感染B淋巴细胞的MHC II类分子（HLA-DQ、-DR和-DP）β链的β1结构域结合，可阻断/改变HLA II类分子/T细胞受体（TCR）的相互作用，并使遗传易感个体（HLA-DRB1和DQB1等位基因）患EBV相关自身免疫性疾病或癌症的易感性增加。导致这些疾病的主要因素包括：EBV感染；HLA II类风险等位基因；性别；以及被EBV潜伏期细胞浸润并形成异位淋巴结构的组织。因此，有必要确定消除具有EBV潜伏期细胞的治疗方法，因为目前的治疗方法（如抗病毒药物和利妥昔单抗）无效。
