Restifo N P, Kawakami Y, Marincola F, Shamamian P, Taggarse A, Esquivel F, Rosenberg S A
Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
J Immunother Emphasis Tumor Immunol. 1993 Oct;14(3):182-90. doi: 10.1097/00002371-199310000-00004.
In this article, we explore the hypothesis that tumor cells can escape recognition by CD8+ T cells via deficiencies in antigen processing and presentation. Aspects of the molecular and cellular biology of major histocompatibility complex class I are reviewed. Evidence for histology-specific molecular mechanisms in the antigen-processing and -presentation deficiencies observed in some human and murine tumors is presented. Mechanisms identified include down-regulation of antigen processing, loss of functional beta 2-microglobulin, and deletion of specific alpha-chain alleles. Finally, we discuss studies using an antigen-presentation-deficient mouse tumor as a model for the immunogenetherapy of an antigen-presentation deficiency.
在本文中，我们探讨了肿瘤细胞可通过抗原加工和呈递缺陷逃避CD8+T细胞识别的假说。回顾了主要组织相容性复合体I类分子和细胞生物学的各个方面。展示了在一些人类和小鼠肿瘤中观察到的抗原加工和呈递缺陷中组织学特异性分子机制的证据。已确定的机制包括抗原加工下调、功能性β2微球蛋白缺失以及特定α链等位基因的缺失。最后，我们讨论了使用抗原呈递缺陷的小鼠肿瘤作为抗原呈递缺陷免疫基因治疗模型的研究。
