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Unité INSERM U343 et Laboratoire d’Immunologie, 06202 Nice cedex 3, France;
* Diaclone research, BP1985, F25020 Besançon cedex, France;
§ Division of Infectious Diseases, Washington University School of Medecine, Saint Louis, Missouri, 63110, USA; and
University of California, San Francisco, San Francisco, California 94143, USA
1Correspondence: Unité INSERM U343, Hôpital de l’Archet 1, Route de St. Antoine de Ginestiere-BP 3079, 06202 Nice cedex 3, France. E-mail: u343{at}hermes.unice.fr
Integrin-associated protein (CD47/IAP) is a pentaspan molecule that
regulates integrin functions. We prepared a CD47-deficient Jurkat T
cell line to assess its role in the arrest of T cells on inflammatory
endothelium. Under flow conditions, constitutive arrest of
CD47-deficient cells is strongly decreased as compared to the original
cell line, whereas reexpression of CD47 reestablishes their ability to
stop. Moreover, cells transfected with a chimera made with the
extracellular portion of CD47 and the transmembrane domain of CD7 or
several truncated forms of CD47 show that the first transmembrane
domain and a short cytoplasmic loop are sufficient for this process.
CD47 effect is indirect and depends mainly on the 
4ß1/VCAM-1
pathway, as shown by blocking antibodies. We detected on endothelium
the two CD47 counter receptors known to date: thrombospondin and
SIRP1. Blocking experiments show that both are involved. Overall,
CD47 participates in the constitutive arrest of T lymphocytes on
inflamed vascular endothelium by up-regulating 4ß1
integrins.—Ticchioni, M., Raimondi, V., Lamy, L., Wijdenes, J.,
Lindberg, F. P., Brown, E. J., Bernard, A.
Integrin-associated protein (CD47/IAP) contributes to T cell arrest on
inflammatory vascular endothelium under flow.
Key Words: adhesion • T cell circulation • integrin
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