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J. Exp. Med.,
Volume 189, Number 3, February 1, 1999 451-460
By
From the * Cardiovascular Research Institute, University of California San Francisco, San Francisco,
California 94143; the Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T
cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells. In mice homozygous for the paucity of lymph node T cell (plt) mutation, naive T cells fail to home to
LNs or the lymphoid regions of spleen. Here we demonstrate that expression of SLC is undetectable in plt mice. In addition to the defect in T cell homing, we demonstrate that dendritic
cells (DCs) fail to accumulate in spleen and LN T cell zones of plt mice. DC migration to LNs
after contact sensitization is also substantially reduced. The physiologic significance of these abnormalities in plt mice is indicated by a markedly increased sensitivity to infection with murine
hepatitis virus. The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal. These findings suggest that the abnormalities in plt mice are
due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T
cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs.
Center for Experimental Medicine and § Laboratory Animal Research Center,
Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan; and the Department of
Immunology, Toho University School of Medicine, Tokyo 143-8540, Japan
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