Stockert E, DeLeo A B, O'Donnell P V, Obata Y, Old L J
J Exp Med. 1979 Jan 1;149(1):200-15. doi: 10.1084/jem.149.1.200.
Normal mouse sera were tested for cytotoxic antibody to surface antigens of cultured monolayer cells infected with AKR-derived ecotropic MuLV, xentropic MuLV, or dualtropic MCF 247 MuLV. Antibody to ecotropic MuLV-infected cells was found in a proportion of C57BL/6, C3Hf/Bi, AKR-Fv-1b, and (C3Hf/Bi X AKR)F1 mice, but not AKR or (AKR X C3Hf/Bi)F1 mice. Antibody to xenotropic MuLV-infected cells was virtually restricted to C57BL/6 mice. Antibody to MCF 247-infected cells was found in all strains tested, including AKR mice. Absorption analysis of (C3Hf/Bi x akr)f1 and AKR-Fv-1b sera with selective reactivity for MCF 247-infected cells showed that these sera recognize distinctive antigens on MCF 247-infected cells that are not present on ecotropic or xenotropic MuLV-infected cells. The transplantable AKR spontaneous leukemia AKSL2 was found to be uniquely sensitive to the cytotoxic action of naturally occurring antibody to MCF 247-related antigens and absorption tests with AKSL2 as the target cell and sera from a single AKR-Fv-1b mouse have permitted the definition of a new MuLV-related cell surface antigen, which has been designated G(AKSL2). Thymocytes from young mice of high leukemia-incidence strains (AKR, C58, and PL) express G(AKSL2), whereas thymocytes from 12 other strains do not. In AKR mice, the antigen is expressed in higher amounts on cells from thymus and bone marrow than on spleen cells. All AKR spontaneous leukemias tested express G(AKSL2), as did three MuLV-induced leukemias arising in G(AKSL2)- strains. Five X-ray-induced leukemias of G(AKSL2)- strains were G(AKSL2)-, as were MuLV+ and MuLV- chemically induced sarcomas. In the limited survey conducted to date, natural antibody to G(AKSL2) has been restricted to strains expressing G(AKSL2) in their normal tissues: AKR, AKR congenic mice AKR-Fv-1b and AKR hybrid mice (C3Hf/Bi x akr)f1 and (C57BL/6 X AKR)F1. In vitro G(AKSL2) induction tests involving MuLV infection of cultured monolayer cells showed that 8 of 12 newly isolated dualtropic MuLV shared the property of G(AKSL2) induction with the prototype MCF MuLV, MCF 247. Of the 12 ecotropic MuLV tested, only the N-tropic MuLV isolated from a leukemia originally induced by Passage A Gross virus induced G(AKSL2). The xenotropic and amphotropic MuLV isolates tested lacked G(AKSL2) inducing activity. Recognition of the g(aksl2) system provides a way to trace the origin and natural history of a class of dualtropic MCF MuLV in the mouse and to determine whether natural antibody to G(AKSL2) plays a role in AKR leukemogenesis.
检测正常小鼠血清中针对感染了源自AKR的嗜亲性MuLV、嗜异性MuLV或双嗜性MCF 247 MuLV的培养单层细胞表面抗原的细胞毒性抗体。在一定比例的C57BL/6、C3Hf/Bi、AKR-Fv-1b以及(C3Hf/Bi×AKR)F1小鼠中发现了针对嗜亲性MuLV感染细胞的抗体,但在AKR或(AKR×C3Hf/Bi)F1小鼠中未发现。针对嗜异性MuLV感染细胞的抗体实际上仅限于C57BL/6小鼠。在所有测试菌株中,包括AKR小鼠,均发现了针对MCF 247感染细胞的抗体。对(C3Hf/Bi×akr)f1和AKR-Fv-1b血清进行吸收分析,这些血清对MCF 247感染细胞具有选择性反应性,结果表明这些血清识别MCF 247感染细胞上独特的抗原,而嗜亲性或嗜异性MuLV感染细胞上不存在这些抗原。可移植的AKR自发性白血病AKSL2被发现对天然存在的针对MCF 247相关抗原的抗体的细胞毒性作用具有独特的敏感性,以AKSL2作为靶细胞并用来自一只AKR-Fv-1b小鼠的血清进行吸收试验,已确定了一种新的与MuLV相关的细胞表面抗原,命名为G(AKSL2)。高白血病发病率菌株(AKR、C58和PL)的幼鼠胸腺细胞表达G(AKSL2),而其他12个菌株的胸腺细胞不表达。在AKR小鼠中,该抗原在胸腺和骨髓细胞上的表达量高于脾细胞。所有测试的AKR自发性白血病均表达G(AKSL2),在G(AKSL2)-菌株中产生的三种MuLV诱导的白血病也表达G(AKSL2)。G(AKSL2)-菌株的五种X射线诱导白血病为G(AKSL2)-,MuLV+和MuLV-化学诱导的肉瘤也是如此。在迄今为止进行的有限调查中,针对G(AKSL2)的天然抗体仅限于在其正常组织中表达G(AKSL2)的菌株:AKR、AKR同源小鼠AKR-Fv-1b以及AKR杂交小鼠(C3Hf/Bi×akr)f1和(C57BL/6×AKR)F1。涉及用MuLV感染培养单层细胞的体外G(AKSL2)诱导试验表明,12种新分离的双嗜性MuLV中有8种与原型MCF MuLV MCF 247具有诱导G(AKSL2)的特性。在测试的12种嗜亲性MuLV中,只有从最初由A株格罗斯病毒诱导的白血病中分离出的N-嗜性MuLV诱导了G(AKSL2)。测试的嗜异性和兼嗜性MuLV分离株缺乏诱导G(AKSL2)的活性。对g(aksl2)系统的识别提供了一种追踪小鼠中一类双嗜性MCF MuLV的起源和自然史的方法,并确定针对G(AKSL2)的天然抗体是否在AKR白血病发生中起作用。