Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse
Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse
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DOI：
10.1073/pnas.97.23.12694
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发表时间：
2000-11-07
影响因子：
11.1
通讯作者：
Cyster, JG
中科院分区：
文献类型：
--
作者：
Luther, SA;Tang, HL;Cyster, JG
自发突变小鼠品系plt/plt缺乏次级淋巴器官趋化因子（SLC）-ser基因，并且破坏了T细胞和树突状细胞（DC）向淋巴组织的运输。我们在这里证明，相关的趋化因子，EB病毒诱导的分子-1配体趋化因子（ELC）的基因，也删除在这个免疫缺陷小鼠品系。使用的方法，包括骨髓重建和双重原位杂交的组合，我们表明，在野生型小鼠中，ELC表达的T区基质细胞，也使SLC。少量的ELC由DC产生，主要是CD 8（+）表型。我们认为表达ELC和SLC的T区基质细胞在将幼稚T细胞和DC聚集在一起以启动免疫应答中起着核心作用。
The spontaneous mutant mouse strain, plt/plt, lacks the secondary lymphoid organ chemokine (SLC)-ser gene and has disrupted trafficking of T cells and dendritic cells (DCs) to lymphoid tissues. We demonstrate here that the gene for the related chemokine, Epstein-Barr virus-induced molecule-1 ligand chemokine (ELC), is also deleted in this immunodeficient mouse strain. Using a combination of approaches, including bone marrow reconstitution and double in situ hybridization, we show in wild-type mice that ELC is expressed by T zone stromal cells that also make SLC. Smaller amounts of ELC are made by DCs, predominantly of the CD8(+) phenotype. We propose that ELC- and SLC-expressing T zone stromal cells play a central role in bringing naive T cells and DCs together for the initiation of immune responses.