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,§
*
First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu, Japan;
Department of Biochemistry, Kobe University School of Medicine, Kobe, Japan;
Department of Biochemistry, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu, Japan;
§
School of Allied Health Science, Faculty of Medicine Osaka University, Osaka, Japan;
¶
Department of Tumor Immunology, University Hospital Nijmegen, Nijmegen, The Netherlands; and
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Department of Physiology, Kobe University School of Medicine, Kobe, Japan
The adhesive function of integrins is regulated through cytoplasmic
signaling. The present study was performed to investigate the relevance
of cytoplasmic signaling and cytoskeletal assembly to integrin-mediated
adhesion induced by chemokines. Adhesion of T cells induced by
chemokines macrophage inflammatory protein (MIP)-1
and MIP-1ß was
inhibited by pertussis toxin, wortmannin, and cytochalasin B,
suggesting that both G protein-sensitive phosphatidylinositol (PI)
3-kinase activation and cytoskeletal assemblies are involved. The
chemokine-induced T cell adhesion could be mimicked by expression of
small G proteins, fully activated H-RasV12, or
H-RasV12Y40C mutant, which selectively binds to PI
3-kinase, in T cells, inducing activated form of LFA-1 and
LFA-1-dependent adhesion to ICAM-1. H-Ras expression also induced
F-actin polymerization which colocalized with profilin in T cells.
Adult T cell leukemia (ATL) cells spontaneously adhered to ICAM-1,
which depended on endogenous MIP-1 and MIP-1ß through activation
of G protein-sensitive PI 3-kinase. H-Ras signal pathway, leading to PI
3-kinase activation, also induced active configuration of LFA-1 and
LFA-1-mediated adhesion of ATL cells, whereas expression of a
dominant-negative H-Ras mutant failed to do. Profilin-dependent
spontaneous polymerization of F-actin in ATL cells was reduced by PI
3-kinase inhibitors. In this paper we propose that H-Ras-mediated
activation of PI 3-kinase can be involved in induction of
LFA-1-dependent adhesion of T cells, which is relevant to
chemokine-mediated signaling, and that profilin may form an important
link between chemokine- and/or H-Ras-mediated signals and F-actin
polymerization, which results in triggering of LFA-1 on T cells or
leukemic T cells.
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