VHL loss is common in clear cell renal cell carcinoma (ccRCC) and triggers a pseudohypoxic state in mutated cells. A study by Jeffrey Rathmell and colleagues now suggests that Vhl deletion also affects the tumour immune-cell infiltrate in RCC.

The myeloid cells that infiltrated Vhl^−/− tumours were also functionally distinct from those in control tumours, as they were more phagocytic ex vivo and had enhanced expression of inflammatory genes and surface markers (including CD11c). Metabolically, Vhl^−/− tumours had higher glucose uptake than controls, and this difference was mainly driven by myeloid cells. Increased expression of CX3C-chemokine ligand 1 (CX3CL1) might be a key alteration in Vhl^−/− cells that drives myeloid cell recruitment, as knocking out Cx3cl1 in these cells reduced the numbers of myeloid cells and their expression of CD11c.

VHL丢失在透明细胞肾细胞癌 (ccRCC) 中很常见，并会引发突变细胞的假缺氧状态。 Jeffrey Rathmell 及其同事的一项研究现在表明， Vhl缺失也会影响 RCC 中的肿瘤免疫细胞浸润。

浸润Vhl ^-/-肿瘤的骨髓细胞在功能上也与对照肿瘤中的细胞不同，因为它们在离体时更具吞噬能力，​​并且炎症基因和表面标志物（包括CD11c）的表达增强。在代谢方面， Vhl ^−/−肿瘤比对照肿瘤具有更高的葡萄糖摄取，这种差异主要是由骨髓细胞驱动的。 CX3C-趋化因子配体 1 (CX3CL1) 表达的增加可能是Vhl ^−/−细胞中驱动骨髓细胞募集的关键改变，因为敲除这些细胞中的Cx3cl1会减少骨髓细胞的数量及其 CD11c 的表达。