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新培育的短命SAM小鼠的免疫反应。IV. 控制辅助性T细胞活性缺陷的基因的染色体定位。

Immune responses in newly developed short-lived SAM mice. IV. Chromosomal location of a gene controlling defective helper T-cell activity.

作者信息

Hanada K, Katoh H, Hosokawa T, Hosono M, Takeda T

机构信息

Department of Senescence Biology, Kyoto University, Japan.

出版信息

Immunology. 1991 Sep;74(1):160-4.

PMID:1834548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1384687/
Abstract

Short-lived SAMP-P/1 mice are low responders in in vitro antibody responses because of a selectively impaired helper T(Th)-cell activity. After crossing with high responders (B10.BR mice), about 12% of (B10.BR x SAM-P/1) (BRP)F2 mice showed low responsiveness, as did SAM-P/1 mice, against two T-dependent antigens, sheep and horse red blood cells (RBC), both of which were not cross-reactive to each other at helper T- and B-cell levels. The immune activities against the two antigens in individual BRPF2 mice showed a good correlation (r = 0.81), thereby suggesting that SAM-P/1 mice have an antigen non-specific Th cell dysfunction. Based on the incidence of the low responders in F2 generation and statistical analyses, the hypo-responsiveness was postulated to be controlled by two genes. To survey the location of these genes, linkage analyses were performed in the F2 mice using a large set of genetic markers. Low responders in the F2 generation showed a significantly higher incidence of SAM-P/1 genotype at the Gpi-1 as well as c locus on chromosome 7 (Chr.7). However, no linkage of low responsiveness to the Hbb locus was evident, an area present at a more distal site to the centromere on the same chromosome. These results suggest that one of the genes controlling the hypo-responsiveness of SAM-P/1 mice is linked to both Gpi-1 and c loci and that it locates at a more proximal site on Chr.7.

摘要

短命的SAMP-P/1小鼠在体外抗体反应中是低反应者,因为其辅助性T(Th)细胞活性存在选择性受损。与高反应者(B10.BR小鼠)杂交后,约12%的(B10.BR×SAM-P/1)(BRP)F2小鼠表现出与SAM-P/1小鼠一样的低反应性,针对两种T细胞依赖性抗原,即绵羊和马红细胞(RBC),这两种抗原在辅助性T细胞和B细胞水平上彼此无交叉反应。个体BRPF2小鼠针对这两种抗原的免疫活性显示出良好的相关性(r = 0.81),从而表明SAM-P/1小鼠存在抗原非特异性Th细胞功能障碍。基于F2代中低反应者的发生率及统计分析,推测这种低反应性受两个基因控制。为了探究这些基因的位置,在F2小鼠中使用大量遗传标记进行了连锁分析。F2代中的低反应者在7号染色体(Chr.7)上的Gpi-1以及c位点处显示出显著更高的SAM-P/1基因型发生率。然而,低反应性与Hbb位点无明显连锁关系,Hbb位点位于同一染色体上着丝粒更远端的区域。这些结果表明,控制SAM-P/1小鼠低反应性的其中一个基因与Gpi-1和c位点均连锁,且位于Chr.7上更靠近近端的位置。

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本文引用的文献

1
A new murine model of accelerated senescence.一种新的加速衰老的小鼠模型。
Mech Ageing Dev. 1981 Oct;17(2):183-94. doi: 10.1016/0047-6374(81)90084-1.
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A rapid method for the isolation of functional thymus-derived murine lymphocytes.一种分离功能性胸腺来源的小鼠淋巴细胞的快速方法。
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Age-related changes in bone mass in the senescence-accelerated mouse (SAM). SAM-R/3 and SAM-P/6 as new murine models for senile osteoporosis.衰老加速小鼠(SAM)骨量的年龄相关性变化。SAM-R/3和SAM-P/6作为老年性骨质疏松症的新小鼠模型。
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Immune responses in newly developed short-lived SAM mice. I. Age-associated early decline in immune activities of cultured spleen cells.新培育的短命衰老加速小鼠(SAM)的免疫反应。I. 培养的脾细胞免疫活性与年龄相关的早期下降。
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Age-related deterioration of ability of acquisition in memory and learning in senescence accelerated mouse: SAM-P/8 as an animal model of disturbances in recent memory.衰老加速小鼠记忆学习获取能力的年龄相关性衰退:SAM-P/8作为近期记忆障碍的动物模型
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Immune responses in newly developed short-lived SAM mice. Selectively impaired T-helper cell activity in in vitro antibody response.新培育的短命衰老加速小鼠(SAM)的免疫反应。体外抗体反应中T辅助细胞活性的选择性受损。
Immunology. 1987 Nov;62(3):425-9.
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Age-related changes in the temporomandibular joint of the senescence accelerated mouse. SAM-P/3 as a new murine model of degenerative joint disease.衰老加速小鼠颞下颌关节的年龄相关性变化。SAM-P/3作为一种新型退行性关节疾病小鼠模型。
Am J Pathol. 1989 Aug;135(2):379-85.
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IL-3 production as a function of age and its correlation with splenomegaly: age versus disease-related change.白细胞介素-3的产生与年龄的关系及其与脾肿大的相关性:年龄与疾病相关变化
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