内膜肉瘤是一种罕见的、侵袭性的肿瘤，由大血管产生。肿瘤免疫微环境的表征可能会提出新的治疗策略。来自 7 名患者的 17 个标本通过免疫组织化学标记为程序性细胞死亡 1 配体 1 (PD-L1)、CD45、CD8、CD4、FOXP3、CD20、CD68 和 LAG3。免疫细胞密度以占肿瘤面积的百分比进行评分（1 [<5%]、2 [5%-50%]、3 [>50%]）；对肿瘤细胞和瘤内免疫细胞的 PD-L1 表达进行评分。使用图像分析软件对免疫标记物密度进行定量。所有内膜肉瘤均显示免疫细胞浸润（41%为1个，53%为2个，6%为3个）。肿瘤细胞和免疫细胞 PD-L1 标记分别见于 35% 和 76% 的病例； PD-L1内膜肉瘤具有较高的CD45、CD8、FOXP3、CD68和白细胞激活基因3（LAG3）细胞密度（P ≤ .01）。同样，免疫细胞上的 PD-L1 表达与较高密度的 CD8 和 FOXP3 细胞相关 (P < .04)。较高的 LAG3 细胞密度与较高的 CD68 细胞密度和坏死相关 (P < .05)。一名生存期延长的患者具有最高的免疫细胞密度和 PD-L1 表达。这些数据表明，内膜肉瘤具有活跃的肿瘤微环境，具有适应性的 PD-L1 表达模式。我们的结果表明免疫疗法可能是一种有效的治疗选择。© 作者 2023。由牛津大学出版社代表美国临床病理学会出版。版权所有。如需权限，请发送电子邮件至：journals.permissions@oup.com。

Intimal sarcomas are rare, aggressive neoplasms that arise from large blood vessels. Characterization of the tumor immune microenvironment may suggest new treatment strategies.Seventeen specimens from 7 patients were labeled by immunohistochemistry for programmed cell death 1 ligand 1 (PD-L1), CD45, CD8, CD4, FOXP3, CD20, CD68, and LAG3. The immune cell density was scored as a percentage of the tumor area (1+ [<5%], 2+ [5%-50%], 3+ [>50%]); PD-L1 expression was scored on tumor cells and on intratumoral immune cells. Immune marker density was quantified using image analysis software.All intimal sarcomas showed immune cell infiltration (41% were 1+, 53% were 2+, 6% were 3+). Tumor and immune cell PD-L1 labeling was seen in 35% and 76% of cases, respectively; PD-L1+ intimal sarcomas had higher CD45+, CD8+, FOXP3+, CD68+, and leukocyte activation gene 3 (LAG3)+ cell densities (P ≤ .01). Similarly, PD-L1 expression on immune cells correlated with higher densities of CD8+ and FOXP3+ cells (P < .04). Higher LAG3+ cell density correlated with higher CD68+ cell density and necrosis (P < .05). One patient with prolonged survival had the highest immune cell density and PD-L1 expression.These data show that intimal sarcomas have an active tumor microenvironment with an adaptive pattern of PD-L1 expression. Our results suggest that immunotherapy may be an effective treatment option.© The Author(s) 2023. Published by Oxford University Press on behalf of American Society for Clinical Pathology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.