Dolcetti R, Giardini R, Doglioni C, Cariati R, Pomponi F, D'Orazi C, Rao S, Lazarovits A I, Butcher E C, Boiocchi M
Division of Experimental Oncology 1, IRCCS, Aviano (PN), Italy.
Am J Pathol. 1997 May;150(5):1595-605.
We have previously shown that the in vivo coordinated expression of individual alpha 4 and beta 7 integrin chains correlated with the leukemic potential displayed by cell lines derived from murine lymphoblastic T-cell lymphomas (T-LBLs) when transplanted subcutaneously into syngeneic AKR mice. In the present study, by using immunofluorescence and immunocytochemical analyses, we have confirmed that the in vivo up-regulation of the alpha 4 beta 7 heterodimeric complex is associated with the leukemic behavior of AKR T-LBLs. In addition, when compared with the parental, highly leukemic NQ22 cells, the variant cell line NQ22V exhibited a reduced leukemic potential that was invariably associated with a delayed alpha 4 beta 7 up-regulation in vivo Moreover, the leukemic cell line SJ-1, derived from a spontaneous T-LBL of the SJL strain, also displayed high levels of alpha 4 beta 7 expression with a pattern of tissue distribution similar to that of NQ22 cells from leukemic AKR animals. Of note, in most of the tissues involved by murine T-LBL dissemination, and particularly in liver, kidney, and lung, alpha 4 beta 7-positive leukemic cells were always located around strongly VCAM-1-positive vascular spaces. These findings are consistent with a possible role of alpha 4 beta 7/VCAM-1 interactions in the extravasation and, consequently, in the leukemic dissemination of murine T-LBL cells. Immunocytochemical analysis carried out in 11 human T-LBLs showed that pathological lymph nodes from all 7 cases with bone marrow infiltration at presentation carried alpha 4 beta 7-positive cells, whereas all 4 aleukemic T-LBLs were repeatedly alpha 4 beta 7 negative, also in metachronous lesions. These findings suggest that alpha 4 beta 7-positive human T-LBLs may represent a distinct clinicopathological entity. In addition, alpha 4 beta 7 expression was significantly more prevalent in younger patients (< 11 years; P = 0.02), further supporting such a hypothesis. Moreover, as in murine T-LBLs, the pattern of alpha 4 beta 7 positivity in involved lymph nodes was mainly focal, whereas nearly all neoplastic cells infiltrating bone marrow expressed this integrin, suggesting a possible role for alpha 4 beta 7 in the leukemic dissemination also of human T-LBLs.
我们之前已经表明,单个α4和β7整合素链的体内协调表达与从小鼠淋巴细胞性T细胞淋巴瘤(T-LBL)衍生的细胞系皮下移植到同基因AKR小鼠时所显示的白血病潜能相关。在本研究中,通过免疫荧光和免疫细胞化学分析,我们证实α4β7异二聚体复合物的体内上调与AKR T-LBL的白血病行为相关。此外,与亲本的、高度白血病性的NQ22细胞相比,变异细胞系NQ22V表现出降低的白血病潜能,这始终与体内α4β7上调延迟相关。此外,源自SJL品系自发性T-LBL的白血病细胞系SJ-1也显示出高水平的α4β7表达,其组织分布模式与白血病AKR动物的NQ22细胞相似。值得注意的是,在大多数受小鼠T-LBL播散累及的组织中,特别是在肝脏、肾脏和肺中,α4β7阳性白血病细胞总是位于强VCAM-1阳性血管周围。这些发现与α4β7/VCAM-1相互作用在渗出以及因此在小鼠T-LBL细胞的白血病播散中可能发挥的作用一致。对11例人类T-LBL进行的免疫细胞化学分析表明,所有7例初诊时有骨髓浸润的病例的病理淋巴结中都有α4β7阳性细胞,而所有4例无白血病的T-LBL在异时性病变中也反复为α4β7阴性。这些发现表明α4β7阳性的人类T-LBL可能代表一种独特的临床病理实体。此外,α4β7表达在年轻患者(<11岁;P = 0.02)中明显更普遍,进一步支持了这一假设。此外,与小鼠T-LBL一样,受累淋巴结中α4β7阳性的模式主要是局灶性的,而几乎所有浸润骨髓的肿瘤细胞都表达这种整合素,这表明α4β7在人类T-LBL的白血病播散中也可能发挥作用。