Pattengale P K, Taylor C R, Twomey P, Hill S, Jonasson J, Beardsley T, Haas M
Am J Pathol. 1982 Jun;107(3):362-77.
Combined clinicopathologic and immunomorphologic evidence is presented that would indicate that a murine leukemia virus (MuLV) with the dualtropic host range is capable of producing a clinically malignant lesion composed of immunoblasts and associated plasma cells in C57BL/6 mice. This process, morphologically diagnosed as an immunoblastic lymphoma of B cells using standard histopathologic criteria, was found to be distinctly polyclonal with regard to immunoglobulin (Ig) isotype when analyzed for both surface and cytoplasmic Ig. Further studies demonstrated that this clinicopathologically malignant, dualtropic MuLV-induced, polyclonal immunoblastic lymphoma of B cells in C57BL/6 mice was normal diploid and unable to be successfully transplanted to nonimmunosuppressed syngeneic recipients. Although all serum heavy and light chain components were found to be progressively elevated as the tumor load increased, the polyclonal increase in serum immunoglobulins was most pronounced for mu heavy and kappa light chains (ie, mu greater than gamma 2A greater than alpha greater than gamma 2B greater than gamma 1; kappa greater than lamba). The dissociation of clinicopathologic and biologic criteria for malignancy in the presently described dualtropic (RadLV) MuLV-induced B-cell lesion is sharply contrasted with the thymotropic (RadLV), MuLV-induced T-cell lymphoblastic lymphoma in C57BL/6 mice. This process is also a clinicopathologically malignant lesion but, when one uses biologic criteria, is found to be distinctly monoclonal, aneuploid, and easily transplanted to nonimmunosuppressed syngeneic recipients. The close clinicopathologic and biologic similarities of the dualtropic MuLV-induced animal model to corresponding human B-cell lymphoproliferative diseases are stressed.
综合临床病理和免疫形态学证据表明，具有双嗜性宿主范围的鼠白血病病毒（MuLV）能够在C57BL/6小鼠中产生由免疫母细胞和相关浆细胞组成的临床恶性病变。使用标准组织病理学标准，该病变在形态学上被诊断为B细胞免疫母细胞淋巴瘤，当分析表面和细胞质免疫球蛋白（Ig）时，发现其在免疫球蛋白（Ig）同种型方面明显为多克隆性。进一步研究表明，C57BL/6小鼠中这种临床病理恶性、双嗜性MuLV诱导的B细胞多克隆免疫母细胞淋巴瘤为正常二倍体，无法成功移植到未免疫抑制的同基因受体中。尽管随着肿瘤负荷增加，所有血清重链和轻链成分均逐渐升高，但血清免疫球蛋白的多克隆增加在μ重链和κ轻链中最为明显（即μ＞γ2A＞α＞γ2B＞γ1；κ＞λ）。目前描述的双嗜性（RadLV）MuLV诱导的B细胞病变中，临床病理和恶性生物学标准的分离与C57BL/6小鼠中嗜胸腺性（RadLV）MuLV诱导的T细胞淋巴母细胞淋巴瘤形成鲜明对比。该病变也是一种临床病理恶性病变，但当使用生物学标准时，发现其明显为单克隆性、非整倍体，且易于移植到未免疫抑制的同基因受体中。强调了双嗜性MuLV诱导的动物模型与相应人类B细胞淋巴增殖性疾病在临床病理和生物学上的密切相似性。
