Published online 15 January 2001.
© The Rockefeller University Press, 0022-1007/2001/1/207/ $5.00
The Journal of Experimental Medicine, Volume 193, Number 2, January 15, 2001 207-218
Mice Lacking Expression of the Chemokines Ccl21-Ser and Ccl19 (plt Mice) Demonstrate Delayed but Enhanced T Cell Immune Responses
Shigeyuki Moria,
Hideki Nakanoa,
Kentaro Aritomia,b,
Chrong-Reen Wangc,
Michael D. Gunnd, and
Terutaka Kakiuchia
a Department of Immunology, Toho University School of Medicine, Tokyo 143-8540, Japan
b Department of Orthopedic Surgery, Juntendo University School of Medicine, Tokyo 113-8421, Japan
c Department of Allergology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan
d Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710
Division of Cardiology, Department of Medicine, Duke University Medical Center, Box 3623, Durham, NC 27710.919-684-8591919-668-0334
nakano{at}duke.edu
The paucity of lymph node T cells (plt) mutation leads to a loss of CCL21 and CCL19 expression in secondary lymphoid organs. plt mice have defects in the migration of naive T cells and activated dendritic cells into the T cell zones of lymphoid organs, suggesting that they would have defects in T cell immune responses. We now demonstrate T cell responses in plt mice are delayed but ultimately enhanced. Responses to contact sensitization are decreased at day 2 after priming but increased at day 6. After subcutaneous immunization, antigen-specific T cell proliferation and cytokine production in plt mice are increased and remain markedly elevated for at least 8 wk. Compared with wild-type mice, a proportion of T cell response in plt mice are shifted to the spleen, and prior splenectomy reduces the T cell response in draining lymph nodes. After immunization of plt mice, T cells and dendritic cells colocalize in the superficial cortex of lymph nodes and in splenic bridging channels, but not in T cell zones. These results demonstrate that plt mice mount robust T cell responses despite the failure of naive T cells and activated dendritic cells to enter the thymus dependent areas of secondary lymphoid organs.
Key Words: chemokines cell migration lymphoid tissue immunomodulators contact hypersensitivity
S. Mori and H. Nakano contributed equally to this work.
H. Nakano's present address is Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC 27710.
C.R. Wang's present address is Department of Internal Medicine, National Cheng Kung University Hospital, 138 Sheng Li Rd., Tainan 700, Taiwan.
Abbreviations used in this paper: BCECF, 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein; CMFDA, 5-chloromethylfluorescein diacetate; DC, dendritic cell; HEV, high endothelial venule; PCl, picryl chloride; plt, paucity of LN T cells; PP, Peyer's patch; WT, wild-type.
© 2001 The Rockefeller University Press

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