一项新的研究发现肿瘤通过CD47-trombospondin-1互动,使免疫性T细胞丧失功能,并阻止它增加癌症治疗的有效性。 A new study finds tumors disable immune T cells via CD47-thrombospondin-1 interaction, and blocking it boosts cancer treatment effectiveness.

在《自然免疫学》上发表的一项新研究表明,肿瘤利用CD47-thrombospondin-1互动,抑制了免疫T细胞,驱使T细胞耗竭并削弱了抗癌反应。 A new study published in Nature Immunology reveals that tumors suppress immune T cells by exploiting a CD47-thrombospondin-1 interaction, driving T cell exhaustion and weakening anti-cancer responses. 研究人员发现,人体和老鼠肿瘤中耗竭的T细胞过量表达的CD47, 与癌症细胞产生的血栓子1结合,进一步抑制了免疫功能。 Researchers found that exhausted T cells in human and mouse tumors overexpress CD47, which binds to thrombospondin-1 produced by cancer cells, further inhibiting immune function. 阻断这种相互作用的称为TAX2恢复T细胞活性,减缓瘤生长黑色素瘤和结直肠癌模型,并提高PD-1检查点抑制剂的有效性. Blocking this interaction with a peptide called TAX2 restored T cell activity, slowed tumor growth in melanoma and colorectal cancer models, and enhanced the effectiveness of PD-1 checkpoint inhibitors. 调查结果表明,一项有希望的新战略是针对这一途径,改进免疫治疗结果。 The findings suggest a promising new strategy to improve immunotherapy outcomes by targeting this pathway.