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DBA小鼠对劳舍尔病毒诱导的白血病的免疫反应。II. 抗原表达与发病机制之间的相关性。

Immune response to Rauscher virus-induced leukemia in DBA mice. II. Correlation between antigenic expression and pathogenesis.

作者信息

Tóth F D, Váczi L

出版信息

Neoplasma. 1978;25(3):265-72.

PMID:79984
Abstract

Previous studies have demonstrated that the Rauscher virus induces a biphasic erythroleukemia in DBA mice, and the regression of the disease is connected with the appearance of antibody-dependent cellular cytotoxicity. In the present work, attempts were made to reveal the mechanism leading to the lethal exacerbation of the leukemia. In the sera of leukemic mice soluble tumor-specific antigen could be demonstrated in the stages of early progression and regression but not in the stage of exacerbation. The antigen was present in form of immune complexes with free antibodies in excess. The emergence of a new population of leukemia cells has been observed during the stage of regression. On the surface of these cells the antigen receptor sites were masked by sialic acid which resulted in the loss of immunosensitivity and immunogenicity.

摘要

先前的研究表明,劳氏病毒可在DBA小鼠中诱发双相性红白血病,且疾病的消退与抗体依赖性细胞毒性的出现有关。在本研究中,我们试图揭示导致白血病致命性加重的机制。在白血病小鼠的血清中,可溶性肿瘤特异性抗原可在疾病早期进展和消退阶段检测到,但在加重阶段则检测不到。该抗原以与过量游离抗体形成免疫复合物的形式存在。在消退阶段观察到了一群新的白血病细胞的出现。在这些细胞表面,抗原受体位点被唾液酸掩盖,导致免疫敏感性和免疫原性丧失。

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