通过靶向肿瘤相关巨噬细胞的嵌合受体工程化溶瘤病毒重振内源性抗肿瘤免疫
Rejuvenating endogenous antitumor immunity via a chimeric receptor-engineered oncolytic virus targeting tumor-associated macrophages.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
PPARα激动剂非诺贝特治疗可提高 CD8(+) T 细胞疗法对黑色素瘤的疗效
英文原题：Treatment with the PPARα agonist fenofibrate improves the efficacy of CD8(+) T cell therapy for melanoma.
查看英文原题
Treatment with the PPARα agonist fenofibrate improves the efficacy of CD8(+) T cell therapy for melanoma.
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中文摘要
过继性转移肿瘤抗原特异性CD8+ T细胞可限制肿瘤进展，但受限于T细胞在肿瘤微环境（TME）中的快速功能损伤。这在一定程度上是由于缺氧和缺糖导致的代谢应激所致。在此，我们报告，对人离体扩增的TIL（肿瘤浸润淋巴细胞）（TILs）进行非诺贝特治疗，可提高其在患者来源异种移植（PDX）小鼠模型中限制黑色素瘤进展的能力。经非诺贝特（一种过氧化物酶体增殖物激活受体α（PPARα）激动剂）处理的TILs，从糖酵解转向脂肪酸氧化（FAO），并增强了在移植新鲜人肿瘤碎片或注射由患者黑色素瘤建立的肿瘤细胞系及离体扩增TILs的小鼠中减缓自体黑色素瘤进展的能力。
展开英文摘要原文
Adoptive transfer of tumor antigen-specific CD8 + T cells can limit tumor progression but is hampered by the T cells' rapid functional impairment within the tumor microenvironment (TME). This is in part caused by metabolic stress due to lack of oxygen and glucose.
Here, we report that fenofibrate treatment of human ex vivo expanded tumor-infiltrating lymphocytes (TILs) improves their ability to limit melanoma progression in a patient-derived xenograft (PDX) mouse model.
TILs treated with fenofibrate, a peroxisome proliferator receptor alpha (PPARα) agonist, switch from glycolysis to fatty acid oxidation (FAO) and increase the ability to slow the progression of autologous melanomas in mice with freshly transplanted human tumor fragments or injected with tumor cell lines established from the patients' melanomas and ex vivo expanded TILs.
论文信息
- 作者
- Hasanpourghadi M、Chekaoui A、Kurian S、Kurupati R、Ambrose R、Giles-Davis W、Saha A、Xiaowei X
- 单位
- The Wistar Institute, Philadelphia, PA 19104, USA.United States
- 期刊
- Molecular therapy oncolytics2023 Dec 19
- 原文标识
- PubMed 38075243 · DOI 10.1016/j.omto.2023.100744
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