Instituto de Investigacion Biosanitaria ibs, 18014 Granada, Spain; Departamento de Bioquimica, Biologia Molecular e Inmunologia III, Facultad de Medicina, Universidad de Granada, Spain.
Servicio de Analisis Clinicos e Inmunologia, UGC Laboratorio Clinico, Hospital Universitario Virgen de las Nieves, 18014 Granada, Spain; Instituto de Investigacion Biosanitaria ibs, 18014 Granada, Spain; Departamento de Bioquimica, Biologia Molecular e Inmunologia III, Facultad de Medicina, Universidad de Granada, Spain.
Curr Opin Immunol. 2018 Apr;51:123-132. doi: 10.1016/j.coi.2018.03.006. Epub 2018 Mar 19.
MHC/HLA class I loss in cancer is one of the main mechanisms of tumor immune escape from T-cell recognition and destruction. Tumor infiltration by T lymphocytes (TILs) and by other immune cells was first described many years ago, but has never been directly and clearly linked to the destruction of HLA-I positive and selection of HLA-I negative tumor cells. The degree and the pattern of lymphocyte infiltration in a tumor nest may depend on antigenicity and the developmental stages of the tumors. In addition, it is becoming evident that HLA-I expression and tumor infiltration have a direct correlation with tumor tissue reorganization. We observed that at early stages (permissive Phase I) tumors are heterogeneous, with both HLA-I positive and HLA-negative cancer cells, and are infiltrated by TILs and M1 macrophages as a part of an active anti-tumor Th1 response. At later stages (encapsulated Phase II), tumor nests are mostly HLA-I negative with immune cells residing in the peri-tumoral stroma, which forms a granuloma-like encapsulated tissue structure. All these tumor characteristics, including tumor HLA-I expression pattern, have an important clinical prognostic value and should be closely and routinely investigated in different types of cancer by immunologists and by pathologists. In this review we summarize our current viewpoint about the alterations in HLA-I expression in cancer and discuss how, when and why tumor HLA-I losses occur. We also provide evidence for the negative impact of tumor HLA-I loss in current cancer immunotherapies, with the focus on reversible ('soft') and irreversible ('hard') HLA-I defects.
MHC/HLA I 类分子在肿瘤中的缺失是肿瘤逃避 T 细胞识别和破坏的主要机制之一。T 淋巴细胞(TIL)和其他免疫细胞浸润肿瘤多年前就已被首次描述,但从未直接明确地与 HLA-I 阳性肿瘤细胞的破坏和 HLA-I 阴性肿瘤细胞的选择联系起来。肿瘤巢中淋巴细胞浸润的程度和模式可能取决于肿瘤的抗原性和发育阶段。此外,越来越明显的是,HLA-I 表达与肿瘤浸润与肿瘤组织重构直接相关。我们观察到,在早期(允许的 I 期),肿瘤是异质性的,既有 HLA-I 阳性的肿瘤细胞,也有 HLA-I 阴性的肿瘤细胞,并且被 TIL 和 M1 巨噬细胞浸润,作为活跃的抗肿瘤 Th1 反应的一部分。在后期(包裹的 II 期),肿瘤巢大多为 HLA-I 阴性,免疫细胞存在于肿瘤周围基质中,形成类似于肉芽肿的包裹组织结构。所有这些肿瘤特征,包括肿瘤 HLA-I 表达模式,都具有重要的临床预后价值,免疫学家和病理学家应在不同类型的癌症中密切和常规地进行研究。在这篇综述中,我们总结了我们目前对肿瘤中 HLA-I 表达改变的观点,并讨论了肿瘤 HLA-I 缺失发生的时间、原因以及如何发生。我们还提供了肿瘤 HLA-I 缺失对当前癌症免疫治疗的负面影响的证据,重点是可逆(“软”)和不可逆(“硬”)HLA-I 缺陷。