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Tumour cell-derived debris and IgG synergistically promote metastasis of pancreatic cancer by inducing inflammation via tumour-associated macrophages

机译:肿瘤细胞来源的碎片和IgG通过与肿瘤相关的巨噬细胞诱导炎症反应协同促进胰腺癌的转移

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摘要

IL-1β released from alternatively activated macrophages stimulated by necrotic cancer cell debris. CD68 , CD163 and CD206 tumour-associated macrophages in the human PDAC samples. Scale bar represents 50 µm. Changes in the mRNA levels of and indicated M2 polarisation of THP-1-derived macrophages in the presence of IL-4/IL-13. Changes in CD68, CD163 and CD206 expression levels indicated M2 polarisation of THP-1-derived macrophages in the presence of PMA and IL-4/IL-13 (superior panel), or M2 polarisation of PBMC-derived macrophages in the presence of M-CSF (inferior panel). The secreted IL-1β level in M2 polarised macrophages derived from THP-1 (left panel) and human PBMCs (right panel) in the presence of IgG and/or BxPC-3 debris. Immunoblotting showing enhanced IL-1β levels in the presence of debris stimulation and IgG. Levels of macrophage phenotypic markers including ARG1, NOS2, MRC1 and CD163 in the presence of IgG, BxPC-3 debris or both. Data are presented as the mean ± SD. **  P
机译:IL-1β从坏死癌细胞碎片刺激的交替激活的巨噬细胞中释放。人类PDAC样品中的CD68,CD163和CD206肿瘤相关巨噬细胞。比例尺代表50μm。在IL-4 / IL-13存在下,THP-1衍生的巨噬细胞的mRNA水平变化和M2极化指示。 CD68,CD163和CD206表达水平的变化表明,在PMA和IL-4 / IL-13(上图)存在下,THP-1衍生的巨噬细胞的M2极化,或在M存在下,PBMC衍生的巨噬细胞的M2极化。 -CSF(下面板)。在存在IgG和/或BxPC-3碎片的情况下,源自THP-1(左图)和人PBMC(右图)的M2极化巨噬细胞中分泌的IL-1β水平。在碎片刺激和IgG存在下,免疫印迹显示IL-1β水平升高。在存在IgG,BxPC-3碎片或两者同时存在的情况下,巨噬细胞表型标记物的水平,包括ARG1,NOS2,MRC1和CD163。数据表示为平均值±SD。 ** P

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