吉西他滨
免疫系统
CD40
癌症研究
胰腺癌
肿瘤微环境
癌症
腺癌
化疗
基质
医学
生物
内科学
免疫学
细胞毒性T细胞
免疫组织化学
体外
生物化学
作者
Gregory L. Beatty,E. Gabriela Chiorean,Matthew Fishman,Babak Saboury,Ursina R. Teitelbaum,Weijing Sun,Richard D. Huhn,Wenru Song,Dongguang Li,Leslie L. Sharp,Drew A. Torigian,Peter J. O’Dwyer,Robert H. Vonderheide
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2011-03-25
卷期号:331 (6024): 1612-1616
被引量:1419
标识
DOI:10.1126/science.1198443
摘要
Immunosuppressive tumor microenvironments can restrain antitumor immunity, particularly in pancreatic ductal adenocarcinoma (PDA). Because CD40 activation can reverse immune suppression and drive antitumor T cell responses, we tested the combination of an agonist CD40 antibody with gemcitabine chemotherapy in a small cohort of patients with surgically incurable PDA and observed tumor regressions in some patients. We reproduced this treatment effect in a genetically engineered mouse model of PDA and found unexpectedly that tumor regression required macrophages but not T cells or gemcitabine. CD40-activated macrophages rapidly infiltrated tumors, became tumoricidal, and facilitated the depletion of tumor stroma. Thus, cancer immune surveillance does not necessarily depend on therapy-induced T cells; rather, our findings demonstrate a CD40-dependent mechanism for targeting tumor stroma in the treatment of cancer.
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