Mosier D E, Yetter R A, Morse H C
J Exp Med. 1985 Apr 1;161(4):766-84. doi: 10.1084/jem.161.4.766.
We have shown that a mixture of murine leukemia viruses (MuLV) causes the acute onset of lymphoproliferation and immunosuppression when injected into adult C57BL/6 mice. The ecotropic/MCF (mink cell focus-inducing) mixture of MuLV stimulates polyclonal B lymphocyte proliferation and differentiation to antibody-secreting cells. Serum Ig levels are elevated for all isotypes except IgA. The viral infection leads to a rapid decline in T lymphocyte responses to mitogens and alloantigens, as well as a decrease in helper cell activity. Specific antibody responses to both T-dependent and T-independent antigens are impaired, and the response of B lymphocytes to mitogens is abolished. The profound immunosuppression seems to be due to the MuLV-induced polyclonal activation of lymphocytes. No active suppression of normal lymphocyte responses by cells from virus-infected mice was observed. The disease induced by the LP-BM5 MuLV isolate thus seems a promising model for the study of lymphocyte activation and the mechanisms of retrovirus-induced immunosuppression.
我们已经证明,将鼠白血病病毒(MuLV)混合物注射到成年C57BL/6小鼠体内会导致淋巴细胞增殖和免疫抑制的急性发作。嗜亲性/MCF(貂细胞集落诱导)MuLV混合物刺激多克隆B淋巴细胞增殖并分化为抗体分泌细胞。除IgA外,所有同种型的血清Ig水平均升高。病毒感染导致T淋巴细胞对丝裂原和同种异体抗原的反应迅速下降,以及辅助细胞活性降低。对T细胞依赖性和T细胞非依赖性抗原的特异性抗体反应受损,并且B淋巴细胞对丝裂原的反应被消除。严重的免疫抑制似乎是由于MuLV诱导的淋巴细胞多克隆激活所致。未观察到病毒感染小鼠的细胞对正常淋巴细胞反应有主动抑制作用。因此,LP-BM5 MuLV分离株诱导的疾病似乎是研究淋巴细胞激活和逆转录病毒诱导的免疫抑制机制的一个有前景的模型。