Coexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in the plt/plt mouse

被引:482
作者
Luther, SA
Tang, HL
Hyman, PL
Farr, AG
Cyster, JG [1 ]
机构
[1] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA
[3] Univ Washington, Dept Biol Struct, Seattle, WA 98195 USA
[4] Univ Washington, Dept Immunol, Seattle, WA 98195 USA
关键词
D O I
10.1073/pnas.97.23.12694
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:12694 / 12699
页数:6
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