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低剂量环磷酰胺联合 IL-2 通过减少调节性 T 细胞、增加 CD8+ T 细胞和 NK 细胞抑制小鼠肿瘤生长

英文原题:Low-dose cyclophosphamide combined with IL-2 inhibits tumor growth by decreasing regulatory T cells and increasing CD8+ T cells and natural killer cells in mice.

查看英文原题

Low-dose cyclophosphamide combined with IL-2 inhibits tumor growth by decreasing regulatory T cells and increasing CD8+ T cells and natural killer cells in mice.

PubMed 2022/03/30(内容时间) Immunobiology Q3 · IF 3.1(JCR 2025)

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中文摘要

白细胞介素-2(IL-2)通过促进细胞毒性效应T细胞的增殖使部分癌症患者获益,但该过程受到调节性T细胞(Tregs)扩增的限制。低剂量环磷酰胺(CTX)可抑制Tregs的数量和功能。我们用Vehicle、CTX、IL-2和CTX + IL-2处理荷癌小鼠,以探究低剂量CTX联合IL-2在抗肿瘤治疗中的作用。与单药治疗相比,CTX + IL-2通过抑制肿瘤细胞增殖和增加凋亡,显著限制了肿瘤生长。CTX + IL-2组肿瘤组织中CD8 + T细胞的浸润显著增加。CTX + IL-2安全地增加了脾脏、淋巴结和外周血中的CD8 + T细胞和NK 细胞,且CTX减弱了IL-2在脾脏中诱导的Tregs增加。

展开英文摘要原文

Interleukin-2 (IL-2) benefits some cancer patients by promoting the proliferation of cytotoxic effector T cells, but this process is limited by the expansion of regulatory T cells (Tregs). Low-dose cyclophosphamide (CTX) can inhibit the number and function of Tregs.

We treated carcinoma-bearing mice with Vehicle, CTX, IL-2 and CTX + IL-2 to investigate the effects of low-dose CTX combined with IL-2 in antitumor treatment. In comparison to monotherapy, CTX + IL-2 significantly limited tumor growth, via tumor cell proliferation inhibition and increased apoptosis.

The infiltration of CD8 + T cells in tumor tissues was significantly increased in the CTX + IL-2 group. CTX + IL-2 safely increased CD8 + T and natural killer cells in the spleen, lymph nodes and peripheral blood, and CTX attenuated the increase in Tregs induced by IL-2 in the spleen.

论文信息

作者
Tang F、Zhong Q、Yang Z、Li H、Pan C、Huang L、Ni T、Deng R
第一作者单位
Department of Medical Oncology, Guizhou Province People's Hospital, Guiyang, Guizhou 550002, China.China
通讯作者单位
Department of Medical Oncology, Guizhou Province People's Hospital, Guiyang, Guizhou 550002, China; NHC Key Laboratory of Pulmonary Immune-related Diseases, Guiyang, Guizhou 550002, China. Electronic address: zhangyu4@gz5055.com.China
文献类型
非美国政府资助研究
期刊
Immunobiology2022 May
原文标识
PubMed 35436750 · DOI 10.1016/j.imbio.2022.152212