Affiliation:
1. From the Department of Immunology, Toho University School of Medicine, Tokyo, Japan; the Laboratory Animal Research Center and Department of Allergology, Institute of Medical Science, University of Tokyo, Tokyo, Japan; and the Department of Laboratory Animal Science, The Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Abstract
Previously, we have shown a mutant mouse DDD/1 with T-cell–specific homing defect that is regulated by an autosomal recessive gene,plt (paucity of lymph node T cells), and seems to be caused by lymph node (LN) stromal cells. In the present study, immunohistochemical analysis showed unusual distribution of T cells in LN, Peyer's patches (PP), and spleen from plt/plt, probably due to the failure of T cells to migrate from blood into the T-cell zone in LN or PP, or into the spleen white pulp across high endothelial venule or marginal zone, respectively, based on the experiments in which labelled T cells were injected intravenously and detected in the tissues. Analysis of surface L-selectin and CD44 suggested that T cells with memory phenotype, probably from afferent lymphatics, recruit intoplt/plt LN. Linkage mapping by simple-sequence length polymorphism of genomic DNA from 190 backcross progenies produced by intercrossing with MSM/Ms, linked plt most closely with D4Mit237, and localized at 24.7 cM from cetromere on chromosome 4. We discuss the possibility that a wild-type gene on plt locus encodes a chemokine inducing T-cell–specific homing into peripheral lymphoid tissues.
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Cited by
172 articles.
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