Premium
T lymphocyte expression of thrombospondin‐1 and adhesion to extracellular matrix components
Author(s) -
Li Shu Shun,
Ivanoff Anna,
Bergström StenErik,
Sandström Anders,
Christensson Birger,
Nerven Joost van,
Holgersson Jan,
Hauzenberger Dan,
Arencibia Ignacio,
Sundqvist KarlGösta
Publication year - 2002
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/1521-4141(200204)32:4<1069::aid-immu1069>3.0.co;2-e
Subject(s) - biology , microbiology and biotechnology , pseudopodia , brefeldin a , fibronectin , cycloheximide , adhesion , extracellular matrix , cell adhesion , cell , biochemistry , golgi apparatus , chemistry , actin , protein biosynthesis , organic chemistry , endoplasmic reticulum
Abstract The mechanisms controlling the formation of pseudopodia and other active cell edges in T lymphocytes are not understood. We show here that T lymphocytes express thrombospondin‐1 (TSP‐1). TSP‐1in T lymphocytes has a high turnover as shown by the fact that brefeldin and monensin rapidly increase while cycloheximide tend to decrease the cellular TSP‐1 content. T cell TSP‐1 is preferentially stored intracellularly and shows variable cell surface expression. T lymphocyte adhesion to fibronectin and collagen type IV induces TSP‐1 expression on the cell surface via a brefeldin sensitive mechanism. A monoclonal antibody to TSP‐1 inhibits the flattening and pseudopodia formation of the adherent T cells. Furthermore, the same antibody to TSP‐1 also exerts an inhibitory effect on T cell migration in the absence of exogenous TSP‐1. These results indicate that endogenous TSP‐1 is part of an adhesion‐dependent mechanism controlling cytoplasmic spreading and migration in T lymphocytes.