RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
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.
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.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
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。
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.
MEMBER ACCOUNT
登录成功会直接打开下一页。