乳腺癌免疫逃逸机理的研究进展

Advances of the Research on Mechanisms of Breast Cancer Escaping from Host Immune Surveillance

目的 综述乳腺癌细胞逃避机体免疫监视机理的研究进展。方法 复习国内、外相关文献 ,从主要组织相容性抗原复合物 (MHC)Ⅰ类分子表型改变、缺乏共刺激信号、肿瘤表达FasL、人类TNF相关凋亡诱导配体(TRAIL)的杀伤作用以及肿瘤抗原诱导机体免疫耐受几个方面对乳腺癌免疫逃逸机理的研究进展加以综述。结果 MHCⅠ类分子表型改变 ,共刺激分子B7缺乏 ,肿瘤细胞表达FasL和TRAIL ,以及肿瘤抗原诱导机体免疫耐受与乳腺癌免疫逃逸有关。结论 乳腺癌细胞通过自身抗原改变、不表达共刺激分子、诱导机体T淋巴细胞凋亡和机体免疫耐受而逃避机体免疫监视 ,但对其免疫逃逸机理中各种因素的相互影响和综合作用尚未被充分认识。

Objective To review the mechanisms of breast cancer escaping from host immune surveillance. Methods The current literatures on the mechanisms of breast cancer cells escaping from host immune surveillance were reviewed in the following aspects: alterations of MHC-Ⅰmolecule phenotype, deficiency of costimulatory molecules, apoptosis of T-lymphocytes induced by breast cancer cells presenting Fas ligand (FasL) and TNF-related apoptosis-inducing ligand (TRAIL) and host immune tolerance induced by tumor cells. Results Loss of classical antigen-presenting human leukocyte antigen (HLA) class-Ⅰmolecules, expression of non-classical HLA class-ⅠmoleculesHLA-G, loss of costimulatory molecule B7, apoptosis of T-lymphocytes induced by tumor cells presenting FasL and TRAIL and antigen-inducing host immune tolerance were related to breast cancer escaping from immune surveillance. Conclusion Breast cancer cells escape from host immune surveillance by altering MHC-Ⅰmolecules, lacking of costimulatory molecules, inducing of apoptosis of T cells and host immune tolerance. But the factors resulting in breast cancer escaping from host immune surveillance are not yet clear and should be further studied.