Girlanda Stefania, Fortis Claudio, Belloni Daniela, Ferrero Elisabetta, Ticozzi Paolo, Sciorati Clara, Tresoldi Moreno, Vicari Aurelio, Spies Thomas, Groh Veronika, Caligaris-Cappio Federico, Ferrarini Marina
Laboratory of Tumor Immunology and Department of Oncology, Istituto di Ricerca e Cura a Carattere Scientifico H.S. Raffaele, Milan, Italy.
Cancer Res. 2005 Aug 15;65(16):7502-8. doi: 10.1158/0008-5472.CAN-05-0731.
Amino-biphosphonates (like pamidronate) activate human Vgamma9/Vdelta2 T lymphocytes and promote their cytotoxicity against multiple myeloma cells. T-cell receptor (TCR)-mediated effector functions of gammadelta cells are enhanced upon triggering of the activating receptor NKG2D by MICA, a stress-inducible antigen expressed by epithelial and some hematopoietic tumors, including multiple myeloma. Here we show that MICA was expressed not only by myeloma cell lines and by 6 of 10 primary multiple myeloma cells from patients but also by bone marrow plasma cells from all (six of six) patients with preneoplastic gammopathy (monoclonal gammopathy of undetermined significance, MGUS), a direct precursor of multiple myeloma. Moreover, compared with multiple myeloma plasma cells, MICA was expressed by MGUS plasma cells at significantly (P < 0.05) higher levels. MICA expressed by myeloma cell lines contributed to killing and IFN-gamma production by Vgamma9/Vdelta2 cells only upon pamidronate treatment, suggesting a dual interaction between Vgamma9/Vdelta2 lymphocytes and multiple myeloma plasma cells involving both TCR triggering and NKG2D-mediated signals. Finally, MICA enhanced killing of freshly derived, pamidronate-treated multiple myeloma cells from patients by gammadelta cells, as indicated by the significantly (P < 0.05) higher gammadelta cytotoxicity against MICA-positive rather than MICA-negative multiple myeloma cells. Our results indicate that MICA expressed by monoclonal plasma cells is functional and correlates with disease stages, suggesting a role for the molecule in the immune surveillance against multiple myeloma. Moreover, pamidronate-activated Vgamma9/Vdelta2 lymphocytes can be exploited in the immune therapy of early stages multiple myeloma and possibly of premalignant disease.
氨基双膦酸盐(如帕米膦酸)可激活人Vγ9/Vδ2 T淋巴细胞,并增强其对多发性骨髓瘤细胞的细胞毒性。上皮细胞和一些造血肿瘤(包括多发性骨髓瘤)表达的应激诱导抗原MICA触发激活受体NKG2D后,γδ细胞的T细胞受体(TCR)介导的效应功能会增强。在此我们表明,MICA不仅在骨髓瘤细胞系以及10例患者来源的原发性多发性骨髓瘤细胞中的6例中表达,而且在所有(6例中的6例)骨髓瘤前期病变(意义未明的单克隆丙种球蛋白病,MGUS)患者的骨髓浆细胞中也有表达,MGUS是多发性骨髓瘤的直接前驱病变。此外,与多发性骨髓瘤浆细胞相比,MGUS浆细胞中MICA的表达水平显著更高(P < 0.05)。骨髓瘤细胞系表达的MICA仅在帕米膦酸处理后才有助于Vγ9/Vδ2细胞的杀伤作用和IFN-γ的产生,这表明Vγ9/Vδ2淋巴细胞与多发性骨髓瘤浆细胞之间存在双重相互作用,涉及TCR触发和NKG2D介导的信号。最后,如对MICA阳性而非MICA阴性的多发性骨髓瘤细胞具有显著更高的γδ细胞毒性(P < 0.05)所示,MICA增强了γδ细胞对患者新鲜分离的、经帕米膦酸处理的多发性骨髓瘤细胞的杀伤作用。我们的结果表明,单克隆浆细胞表达 的MICA具有功能,且与疾病阶段相关,提示该分子在针对多发性骨髓瘤的免疫监视中发挥作用。此外,帕米膦酸激活的Vγ9/Vδ2淋巴细胞可用于早期多发性骨髓瘤以及可能的癌前疾病的免疫治疗。