REPROGRAMMING IMMUNE ENVIRONMENT IN BREAST CANCER VIA DENDRITIC CELLS
    1.
    发明申请
    REPROGRAMMING IMMUNE ENVIRONMENT IN BREAST CANCER VIA DENDRITIC CELLS 审中-公开
    通过感染细胞转染乳腺癌免疫环境

    公开(公告)号:US20130064855A1

    公开(公告)日:2013-03-14

    申请号:US13611976

    申请日:2012-09-12

    摘要: Compositions and methods for the treatment of cancer disclosed herein. The method of the present invention comprises administration of compositions comprising β-glucan, a natural ligand for dectin-1, to block OX40L expression on tumor associated mDCs by blocking STAT6 phosphorylation. The β-glucan-treated mDCs secrete higher levels of IL-12p70 and do not expand TNFα and IL-13-producing CD4+ T cells, further resulting in inhibition of Th2 responses. Thus, compositions disclosed herein reprogram the function of mDCs in breast tumor microenvironment and turn tumor promoting Th2-type chronic inflammation into Th1-type acute inflammation that are able to reject tumors. The present invention finds particular uses for the intratumoral administration of the composition thereby directly binding to and directing a Th1-type acute inflammation.

    摘要翻译: 本文公开的用于治疗癌症的组合物和方法。 本发明的方法包括施用包含葡聚糖的组合物,其是dectin-1的天然配体,通过阻断STAT6磷酸化阻断肿瘤相关mDC上的OX40L表达。 葡聚糖处理的mDC分泌更高水平的IL-12p70,不扩大TNFα和IL-13产生的CD4 + T细胞,进一步导致Th2应答的抑制。 因此,本文公开的组合物重新编码mDC在乳腺肿瘤微环境中的功能,并将肿瘤促进Th2型慢性炎症转化为能够排斥肿瘤的Th1型急性炎症。 本发明特别用于肿瘤内施用组合物,从而直接结合并导向Th1型急性炎症。