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小鼠对弗氏病毒白血病的遗传抗性机制。IV. 体外调节免疫抑制的基因(Fv-3)的鉴定及其与Fv-2和调节骨髓同种异体移植反应性的基因的区别。

Mechanisms of genetic resistance to Friend virus leukemia in mice. IV. Identification of a gene (Fv-3) regulating immunosuppression in vitro, and its distinction from Fv-2 and genes regulating marrow allograft reactivity.

作者信息

Kumar V, Goldschmidt L, Eastcott J W, Bennett M

出版信息

J Exp Med. 1978 Feb 1;147(2):422-33. doi: 10.1084/jem.147.2.422.

Abstract

Friend leukemia viru (FV) suppresses the proliferative response of normal lymphocytes to mitogens. The in vitro suppressive effect of FV on lymphocyte mitogenesis is mediated by T-suppressor cells and is under host genetic control. Lymphocytes from strains of mice of the C57BL background (e.g., C57BL/6) are resistant while cells from other strains (e.g., 129 and DBA/2) are susceptible. Genetic analyses utilizing resistant and susceptible parental strains, their F1, intercross and backcross progeny indicated that susceptibility to in vitro suppression is regulated by a single autosomal gene, dominant for susceptibility to suppression. This gene, which is not linked to the H-2 complex, segregated independently of the Fv-2 gene which controls resistance to spleen focus formation in vivo. The gene is also unlinked to the Ir-like genes which regulate the ability of H-2d mice to reject H-2b bone marrow grafts. The gene is therefore designated as Fv-3. Fv-3 may mediate its effect by regulating the numbers and/or functions of T-suppressor cells.

摘要

Friend白血病病毒(FV)可抑制正常淋巴细胞对有丝分裂原的增殖反应。FV对淋巴细胞有丝分裂的体外抑制作用由T抑制细胞介导,并受宿主基因控制。C57BL背景的小鼠品系(如C57BL/6)的淋巴细胞具有抗性,而其他品系(如129和DBA/2)的细胞则易感。利用抗性和易感亲本品系、它们的F1、杂交和回交后代进行的遗传分析表明,体外抑制的易感性由一个常染色体基因调控,该基因对抑制易感性呈显性。这个基因与H-2复合体不连锁,与控制体内对脾集落形成抗性的Fv-2基因独立分离。该基因也与调节H-2d小鼠排斥H-2b骨髓移植能力的Ir样基因不连锁。因此,该基因被命名为Fv-3。Fv-3可能通过调节T抑制细胞的数量和/或功能来介导其作用。

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