Wang Jun, Chen Lieping
Department of Immunobiology and Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut, USA.
Department of Immunobiology and Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut, USA.
J Invest Dermatol. 2014 Nov;134(11):2675-2677. doi: 10.1038/jid.2014.251.
An immune-suppressive role of myeloid-derived suppressor cells (MDSCs) in melanoma has long been speculated, whereas molecular mechanisms underlying this role are not well understood. Here, Chung and colleagues show that dendritic cell-associated, heparan sulfate proteoglycans-dependent integrin ligand (DC-HIL), a cell surface immune-modulatory molecule, is highly expressed on tumor-associated MDSCs. Genetic ablation or antibody blockade of DC-HIL delays the growth of transplantable B16 melanoma in syngeneic mice, which is accompanied by enhanced antitumor T-cell activities. These findings support a role for DC-HIL in immune evasion within the melanoma microenvironment.
长期以来,人们一直推测髓系来源的抑制性细胞(MDSCs)在黑色素瘤中具有免疫抑制作用,然而其潜在的分子机制尚未完全明确。在此,Chung及其同事表明,树突状细胞相关的硫酸乙酰肝素蛋白聚糖依赖性整合素配体(DC-HIL),一种细胞表面免疫调节分子,在肿瘤相关的MDSCs上高度表达。对DC-HIL进行基因敲除或抗体阻断可延缓同基因小鼠体内可移植性B16黑色素瘤的生长,同时伴有抗肿瘤T细胞活性增强。这些发现支持了DC-HIL在黑色素瘤微环境免疫逃逸中的作用。