CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Epithelial ovarian cancer is infiltrated by activated effector T cells co-expressing CD39, PD-1, TIM-3, CD137 and interacting with cancer cells and myeloid cells.
Epithelial ovarian cancer is infiltrated by activated effector T cells co-expressing CD39, PD-1, TIM-3, CD137 and interacting with cancer cells and myeloid cells.
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这些数据表明，EOC 中富集了 CD137 + CD39 + PD-1 + TIM-3 + CD45RA - CD62L - CD95 + T 淋巴细胞，这一表型可能受到肿瘤细胞上的抗原识别以及由浸润性髓系细胞主要提供的一系列抑制性和共刺激信号的共同调控。
本观察性研究采用免疫组织化学、基因表达谱分析和流式细胞术，分析48份EOC样本的抗原谱及免疫组成，重点关注TIL（肿瘤浸润淋巴细胞）。
具有部分耗竭特征的活化T细胞，仅见于EOC样本，而在相应外周血或腹水中未见，其表面表型为CD137+CD39+PD-1+TIM-3+CD45RA-CD62L-CD95+，提示肿瘤微环境可能维持这一特殊表型。有趣的是，肿瘤细胞表达多种可能刺激肿瘤特异性TIL的肿瘤相关抗原；巨噬细胞则同时提供共刺激和抑制信号，且在富含TIL、具有上述CD137+CD39+PD-1+TIM-3+CD45RA-CD62L-CD95+特征的样本中更丰富。
EOC中富集CD137+CD39+PD-1+TIM-3+CD45RA-CD62L-CD95+ T淋巴细胞，其表型可能受肿瘤细胞抗原识别以及浸润髓系细胞提供的抑制和共刺激信号共同调节。研究还发现了可能抑制局部免疫、且可作为免疫治疗靶点的通路。
In this observational study we analyzed by immunohistochemistry, gene expression profiling and flow cytometry the antigenic landscape and immune composition of 48 EOC specimens, with a focus on tumor-infiltrating lymphocytes (TILs).
Activated T cells showing features of partial exhaustion with a CD137 + CD39 + PD-1 + TIM-3 + CD45RA - CD62L - CD95 + surface profile were exclusively present in EOC specimens but not in corresponding peripheral blood or ascitic fluid, indicating that the tumor microenvironment might sustain this peculiar phenotype. Interestingly, while neoplastic cells expressed several tumor-associated antigens possibly able to stimulate tumor-specific TILs, macrophages provided both co-stimulatory and inhibitory signals and were more abundant in TILs-enriched specimens harboring the CD137 + CD39 + PD-1 + TIM-3 + CD45RA - CD62L - CD95 + signature.
These data demonstrate that EOC is enriched in CD137 + CD39 + PD-1 + TIM-3 + CD45RA - CD62L - CD95 + T lymphocytes, a phenotype possibly modulated by antigen recognition on neoplastic cells and by a combination of inhibitory and co-stimulatory signals largely provided by infiltrating myeloid cells. Furthermore, we have identified immunosuppressive pathways potentially hampering local immunity which might be targeted by immunotherapeutic approaches.
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