Open AccessCoexpression of the chemokines ELC and SLC by T zone stromal cells and deletion of the ELC gene in theplt/pltmouse
Author(s) -
Sanjiv A. Luther,
Hao Tang,
Paul Hyman,
Andrew G. Farr,
Jason G. Cyster
Publication year - 2000
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.97.23.12694
Subject(s) - stromal cell , biology , chemokine , cd8 , immune system , phenotype , bone marrow , microbiology and biotechnology , gene , immunology , cancer research , genetics
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 doublein 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.