A novel mutant gene involved in T-lymphocyte-specific homing into peripheral lymphoid organs on mouse chromosome 4
A novel mutant gene involved in T-lymphocyte-specific homing into peripheral lymphoid organs on mouse chromosome 4
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DOI：
10.1182/blood.v91.8.2886.2886_2886_2895
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发表时间：
1998-04-15
期刊：
影响因子：
20.3
通讯作者：
Kakiuchi, T
中科院分区：
文献类型：
--
作者：
Nakano, H;Mori, S;Kakiuchi, T
以前，我们已经显示了突变的小鼠DDD/1与T细胞特异性归巢缺陷，是由常染色体隐性基因，坑（淋巴结T细胞的缺乏），似乎是由淋巴结（LN）基质细胞。在本研究中，免疫组织化学分析显示LN、派伊尔集合淋巴结（PP）和plt/plt脾中T细胞的异常分布，可能是由于T细胞无法从血液迁移到LN或PP的T细胞区，或分别穿过高内皮微静脉或边缘区进入脾白色髓，这是基于将标记的T细胞静脉注射并在组织中检测的实验。表面L-选择素和CD 44的分析表明，具有记忆表型的T细胞，可能来自传入神经，募集到plt/plt LN。通过简单序列长度多态性的基因组DNA的连锁图谱从190回交后代与MSM/Ms，连锁坑最密切的D4 Mit 237，并定位在24.7 cM的第4染色体上的cetromere。我们讨论的可能性，野生型基因的坑位点编码的趋化因子诱导T细胞特异性归巢到外周淋巴组织。(C)1998年，美国血液学会。
Previously, we have shown a mutant mouse DDD/1 with T-cell-specific homing defect that is regulated by an autosomal recessive gene, pit (paucity of lymph node T cells), and seems to be caused by lymph node (LN) stromal cells. In the present study, immunohistochemical analysis showed unusual distribution of T cells in LN, Peyer's patches (PP), and spleen from plt/plt, probably due to the failure of T cells to migrate from blood into the T-cell zone in LN or PP, or into the spleen white pulp across high endothelial venule or marginal zone, respectively, based on the experiments in which labelled T cells were injected intravenously and detected in the tissues. Analysis of surface L-selectin and CD44 suggested that T cells with memory phenotype, probably from afferent lymphatics, recruit into plt/plt LN. Linkage mapping by simple-sequence length polymorphism of genomic DNA from 190 backcross progenies produced by intercrossing with MSM/Ms, linked pit most closely with D4Mit237, and localized at 24.7 cM from cetromere on chromosome 4. We discuss the possibility that a wild-type gene on pit locus encodes a chemokine inducing T-cell-specific homing into peripheral lymphoid tissues. (C) 1998 by The American Society of Hematology.