黑色素瘤
趋化因子
肿瘤微环境
癌症研究
干扰素
免疫学
医学
免疫疗法
干扰素β
细胞毒性T细胞
免疫系统
巨噬细胞
干扰素γ
生物
体外
生物化学
作者
Aya Kakizaki,Taku Fujimura,Sadanori Furudate,Yumi Kambayashi,Takeshi Yamauchi,Hideo Yagita∥,Setsuya Aiba
出处
期刊:OncoImmunology
[Informa]
日期:2015-05-26
卷期号:4 (11): e1047584-e1047584
被引量:72
标识
DOI:10.1080/2162402x.2015.1047584
摘要
An imbalance of immunosuppressive cells and cytotoxic cells plays an important role in the tumor-bearing host. Together with regulatory T cells (Tregs), tumor-associated macrophages (TAMs) play roles in maintaining the tumor microenvironment. Since interferon beta (IFN-β) has been clinically used for the treatment of malignant melanoma, we investigated the immunomodulatory effect of IFN-β during melanoma growth to elucidate the effects of IFN-β on the tumor microenvironment by using the B16F10 melanoma model. Peritumorally administered IFN-β significantly decreased the mRNA expression and production of Th2-related chemokines, which suppressed the recruitment of Tregs in B16F10 melanoma. Since the administration of IFN-β augments the expression of PD-1 on TILs, the co-administration of anti-PD-1 Ab augmented the therapeutic effect of IFN-β for the treatment of B16F10 melanoma. Moreover, in parallel with the mouse model, in the human system, IFN-β decreased the production of Th2-related chemokines and augmented the production of Th1-related chemokines from monocyte-derived M2 macrophages. Since these immunomodulatory effects of IFN-β on macrophages were also observed in the lesional skin of human in-transit melanoma, our present data suggest one of the possible immunomodulatory effects of IFN-β and support the possibility of IFN-β in combination with anti-PD-1 Ab for the treatment of melanoma.
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