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针对莫洛尼病毒诱导的淋巴瘤(YAC)的抗体反应和自然杀伤细胞活性的遗传变异。

Genetic variation in antibody response and natural killer cell activity against a Moloney virus-induced lymphoma (YAC).

作者信息

Asjö B, Kiessling R, Klein G, Povey S

出版信息

Eur J Immunol. 1977 Aug;7(8):554-8. doi: 10.1002/eji.1830070812.

Abstract

Antibody formation against the Moloney virus-determined surface antigen (MCSA) was found to be under genetic control. In the (A X C57BL)F1 cross one dominant gene played a major role, resulting in bimodal distribution of the antibody response. This gene showed no linkage to H-2, IgG heavy chain immunoglobulin allotype, the coat color markers B and C, and five different isozyme markers representing chromosome numbers 1, 4, 7, 8 and 9. Antibody response to MCSA was not correlated with antibody titers against the virion proteins, confirming that MCSA was an independent entity. There was no relationship between the segregation of natural killer cell activity and antibody response in a [(A X C57BL) X A] backcross population.

摘要

发现针对莫洛尼病毒决定的表面抗原(MCSA)的抗体形成受基因控制。在(A×C57BL)F1杂交中,一个显性基因起主要作用,导致抗体反应呈双峰分布。该基因与H-2、IgG重链免疫球蛋白同种异型、毛色标记B和C以及代表染色体1、4、7、8和9的五个不同同工酶标记均无连锁关系。对MCSA的抗体反应与针对病毒粒子蛋白的抗体滴度无关,证实MCSA是一个独立的实体。在[(A×C57BL)×A]回交群体中,自然杀伤细胞活性的分离与抗体反应之间没有关系。

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