Grandér D, Xu B, Wang P, Einhorn S
Division for Experimental Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.
Leukemia. 1994 Feb;8(2):299-304.
Both gamma- and alpha-interferons (IFNs) have been shown to induce clinical responses in chronic myelogenous leukemia (CML). The mechanisms behind these effects are not known. In chronic phase CML, granulocytic progenitors normally found in the bone marrow only, are found extramedullary. A defect in the adhesion of CML cells, that may be responsible for this finding, has been described earlier. In this study, we have investigated whether IFN can restore the defect in CML cell adhesion. It was found that gamma-, but not alpha-IFN, strongly induced the adhesion of CML cells to other cells and to plastic in a majority of the patients. In parallel, an induction in the expression of the adhesion molecules ICAM-1 and LFA-1 was found, and blocking of these molecules by antibodies abolished the effect. The ability of gamma-IFN to restore the adhesive property of CML cells may add to the antitumor effects observed with gamma-IFN therapy in CML.
γ干扰素和α干扰素均已被证明可在慢性粒细胞白血病(CML)中诱导临床反应。这些效应背后的机制尚不清楚。在慢性期CML中,通常仅存在于骨髓中的粒细胞祖细胞在髓外被发现。先前已描述过CML细胞黏附缺陷可能是这一发现的原因。在本研究中,我们调查了干扰素是否能恢复CML细胞黏附缺陷。结果发现,在大多数患者中,γ干扰素而非α干扰素能强烈诱导CML细胞与其他细胞及塑料的黏附。同时,发现黏附分子ICAM-1和LFA-1的表达有所诱导,并且用抗体阻断这些分子可消除该效应。γ干扰素恢复CML细胞黏附特性的能力可能会增强γ干扰素治疗CML时观察到的抗肿瘤效应。