Marshall D J, Gaulton G N
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, USA.
Leukemia. 1996 Dec;10(12):1860-6.
Although the exact mechanisms of murine leukemia virus (MuLV)-induced lymphomagenesis have yet to be elucidated, it is clear that the immune reponse to viral proteins plays a critical role in this disease process. The parameters for lymphomagenesis are governed by an inverse relationship between viral persistence and immune responsiveness. MuLV have evolved ways to avoid immune detection either by altering their own genome or by altering the host environment. In addition, the intrathymic replication of MuLV during thymocyte maturation and immune selection plays an important role in T cell repertoire development and immune inhibition. These viruses have served as a highly effective experimental model in understanding the many pathways by which MuLV have overcome immune detection and thereby led to lymphomagenesis.
尽管鼠白血病病毒(MuLV)诱导淋巴瘤发生的确切机制尚未阐明,但很明显,对病毒蛋白的免疫反应在这一疾病过程中起着关键作用。淋巴瘤发生的参数由病毒持续性和免疫反应性之间的反比关系决定。MuLV已经进化出通过改变自身基因组或改变宿主环境来避免免疫检测的方法。此外,MuLV在胸腺细胞成熟和免疫选择过程中的胸腺内复制在T细胞库发育和免疫抑制中起重要作用。这些病毒已成为理解MuLV克服免疫检测并由此导致淋巴瘤发生的多种途径的高效实验模型。