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CD43 Plays Both Antiadhesive and Proadhesive Roles in Neutrophil Rolling in a Context-Dependent Manner¹

Masanori Matsumoto^*,, Akiko Shigeta^*, Masayuki Miyasaka and Takako Hirata^2,*

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

As the first step in the recruitment of neutrophils into tissues, the cells become tethered to and roll on the vessel wall. These processes are mediated by interactions between the P- and E-selectins, expressed on the endothelial cells of the vessel wall, and their ligands, expressed on the neutrophils. Recently, we reported that CD43 on activated T cells functions as an E-selectin ligand and thereby mediates T cell migration to inflamed sites, in collaboration with P-selectin glycoprotein ligand-1 (PSGL-1), a major P- and E-selectin ligand. Here, we examined whether CD43 on neutrophils also functions as an E-selectin ligand. CD43 was precipitated with an E-selectin-IgG chimera from mouse bone marrow neutrophils. A CD43 deficiency diminished the E-selectin-binding activity of neutrophils when PSGL-1 was also deficient. Intravital microscopy showed that the CD43 deficiency significantly increased leukocyte rolling velocities in TNF--stimulated venules blocked with an anti-P-selectin mAb, where the rolling was mostly E-selectin dependent, when PSGL-1 was also absent. In contrast, in venules with trauma-induced inflammation, where the rolling was largely P-selectin dependent, the CD43 deficiency reduced leukocyte rolling velocities. Collectively, these observations suggest that CD43 generally serves as an antiadhesive molecule to attenuate neutrophil-endothelial interactions, but when E-selectin is expressed on endothelial cells, it also plays a proadhesive role as an E-selectin ligand.

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, a grant-in-aid for Scientific Research from the Japan Society for the Promotion of Science, and a Long-Range Research Initiative grant from the Japan Chemical Industry Association.

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: PSGL-1, P-selectin glycoprotein ligand-1; sLe^X, sialyl Lewis^X; ESL-1, E-selectin ligand-1; WT, wild type; DKO, PSGL-1 and CD43 double-knockout; B6, C57BL/6J; BM, bone marrow; SA-HRP, HRP-conjugated streptavidin.