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CD43 Collaborates with P-Selectin Glycoprotein Ligand-1 to Mediate E-Selectin-Dependent T Cell Migration into Inflamed Skin¹

Masanori Matsumoto^*,, Akiko Shigeta^*, Yuko Furukawa^*,, Toshiyuki Tanaka, Masayuki Miyasaka and Takako Hirata^2,*

^* The 21st Century Center of Excellence Program, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan; and Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

Activated T cell migration into nonlymphoid tissues is initiated by the interactions of P- and E-selectin expressed on endothelial cells and their ligands on T cells. P-selectin glycoprotein ligand-1 (PSGL-1) has been the only E-selectin ligand demonstrated to function during the in vivo migration of activated T cells. We show in this study that CD43-deficient Th1 cells, like PSGL-1-deficient cells, exhibited reduced E-selectin-binding activity compared with wild-type cells. Th1 cells with a PSGL-1 and CD43 double deficiency showed even less E-selectin-binding activity. In migration assays in which adoptively transferred cells migrate to inflamed skin P- and E-selectin dependently, CD43 contributed significantly to PSGL-1-independent Th1 cell migration. In addition, in vivo activated T cells from the draining lymph nodes of sensitized mice deficient in PSGL-1 and/or CD43 showed significantly decreased E-selectin-binding activity and migration efficiency, with T cells from double-deficient mice showing the most profound decrease. Collectively, these results demonstrate that the CD43 expressed on activated T cells functions as an E-selectin ligand and thereby mediates T cell migration to inflamed sites, in collaboration with PSGL-1.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by a grant-in-aid for the 21st Century Center of Excellence Program from the Ministry of Education, Culture, Sports, Science and Technology, Japan, and a grant-in-aid for scientific research from the Japan Society for the Promotion of Science, Japan.

² Address correspondence and reprint requests to Dr. Takako Hirata, The 21st Century Center of Excellence Program, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan. E-mail address: thirata{at}biken.osaka-u.ac.jp

³ Abbreviations used in this paper: LN, lymph node; CHS, contact hypersensitivity; ESL-1, E-selectin ligand-1; DKO, PSGL-1/CD43 double deficient; LCMV, lymphocytic choriomeningitis virus; PSGL-1, P-selectin glycoprotein ligand-1; SA, streptavidin; sLe^X, sialyl Lewis^X; WT, wild type.

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