We read with great interest the article by Zhang et al 1 showing that CD8+ cell infiltration in pancreatic tumours can be enhanced by depletion of myeloid cells (CD11b+ macrophages and myeloid-derived suppressor cells) and that the depletion of CD11b+ cells resulted in decreased PD-L1 expression on cancer cells thus impairing the triggering of the inhibitory receptor PD-1 on T cells.1 Recruitment and activation of CD8+ lymphocytes in tumours are suppressed by mechanisms only partially understood and rescuing CD8+ cell infiltrate in tumours is one of the objectives of immunotherapies.1 2 Tumour-associated macrophages (TAMs) play a crucial role in the relation between tumour cells and their environment.3 Here, we confirm the interplay between macrophages and CD8+ cells in pancreatic cancer and identify a potential way to exploit this enhancing effect of anti-PD-1 treatment. Indeed, we show that reduction of macrophage infiltrate, through treatment with an anti-Bcl-2-Associated athanoGene 3 (BAG3) antibody,4 results in increased number of CD8+ cells in pancreatic tumours in a murine model. BAG3 is a co-chaperone of …

中文翻译：

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抗BAG3和抗PD-1治疗对胰腺癌巨噬细胞浸润、CD8+T细胞数量和肿瘤生长的联合作用

我们证实了胰腺癌中巨噬细胞和 CD8+ 细胞之间的相互作用，并确定了一种利用抗 PD-1 治疗的这种增强作用的潜在方法。事实上，我们表明，通过用抗 Bcl-2 相关 athanoGene 3 (BAG3) 抗体治疗，巨噬细胞浸润减少 4 导致小鼠模型胰腺肿瘤中 CD8+ 细胞的数量增加。BAG3 是……的共同伴侣