CAR-T（CAR-T）细胞疗法在非肿瘤性疾病中的应用
Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.
CAR-T（CAR-T）细胞在血液系统恶性肿瘤中的应用推动了这种免疫治疗形式的显著进展。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
用于研究 TAM 对肿瘤免疫治疗调控的离体 3D 肿瘤微环境模拟培养
英文原题：An Ex Vivo 3D Tumor Microenvironment-Mimicry Culture to Study TAM Modulation of Cancer Immunotherapy.
查看英文原题
An Ex Vivo 3D Tumor Microenvironment-Mimicry Culture to Study TAM Modulation of Cancer Immunotherapy.
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中文摘要
肿瘤相关巨噬细胞（TAMs）在实体瘤微环境（TME）中积聚，并已被证明可促进肿瘤生长并抑制抗肿瘤免疫反应。TAM介导的对T细胞抗肿瘤反应性的抑制被认为是许多免疫疗法的主要障碍，包括免疫检查点阻断和过继性T/CAR-T 细胞疗法。一种能够密切模拟TME的离体培养系统可以极大地促进癌症免疫疗法的研究。在此，我们报道了一种3D TME模拟培养的开发，该培养由人TME的三个主要组分构成，包括人肿瘤细胞、TAMs和肿瘤抗原特异性T细胞。这种TME模拟培养能够读出TAM介导的对T细胞抗肿瘤反应性的抑制，因此可用于研究TAM对基于T细胞的癌症免疫疗法的调节。作为原理验证，进行了PD-1/PD-L1阻断疗法和MAO-A阻断疗法的研究并得到验证。
展开英文摘要原文
Tumor-associated macrophages (TAMs) accumulate in the solid tumor microenvironment (TME) and have been shown to promote tumor growth and dampen antitumor immune responses. TAM-mediated suppression of T-cell antitumor reactivity is considered to be a major obstacle for many immunotherapies, including immune checkpoint blockade and adoptive T/CAR-T-cell therapies. An ex vivo culture system closely mimicking the TME can greatly facilitate the study of cancer immunotherapies.
Here, we report the development of a 3D TME-mimicry culture that is comprised of the three major components of a human TME, including human tumor cells, TAMs, and tumor antigen-specific T cells. This TME-mimicry culture can readout the TAM-mediated suppression of T-cell antitumor reactivity, and therefore can be used to study TAM modulation of T-cell-based cancer immunotherapy. As a proof-of-principle, the studies of a PD-1/PD-L1 blockade therapy and a MAO-A blockade therapy were performed and validated.
论文信息
- 作者
- Li YR、Yu Y、Kramer A、Hon R、Wilson M、Brown J、Yang L
- 单位
- Department of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA 90095, USA.United States
- 文献类型
- 非美国政府资助研究
- 期刊
- Cells2022 May 8
- 原文标识
- PubMed 35563889 · DOI 10.3390/cells11091583
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