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This Article Full Text Full Text (PDF) All Versions of this Article: fj.07-9268comv1 22/3/682    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Norling, L. V. Articles by Perretti, M. PubMed PubMed Citation Articles by Norling, L. V. Articles by Perretti, M.

Inhibitory control of endothelial galectin-1 on in vitro and in vivo lymphocyte trafficking

William Harvey Research Institute, Barts, and The London, Charterhouse Square, London, UK

¹Correspondence: The William Harvey Research Institute, Barts, and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK. E-mail: m.perretti{at}qmul.ac.uk

Galectin-1 (Gal-1) is a β-galactoside-binding protein, the expression of which is increased in endothelial cells on exposure to proinflammatory stimuli. Through binding of several receptors (CD7, CD45, and CD43) Gal-1 is known to induce apoptosis of activated T lymphocytes, an effect thought to mediate the beneficial effects it exerts in various inflammatory models. The data presented here highlights another function for Gal-1, that of a negative regulator of T-cell recruitment to the endothelium under both physiological and pathophysiological conditions. We have shown, using siRNA to knockdown Gal-1 in endothelial cells, that endogenous Gal-1 limits T-cell capture, rolling, and adhesion to activated endothelial cells under flow. Furthermore, the reverse effect is observed when exogenous human recombinant Gal-1 is added to activated endothelial monolayers whereby a dramatic reduction in lymphocyte recruitment is seen. These findings are corroborated by studies in Gal-1 null mice in which homing of wild-type (WT) T lymphocytes is significantly increased to mesenteric lymph nodes and to the inflamed paw in a model of delayed-type hypersensitivity. In conclusion, mimicking endothelial Gal-1 actions would be a novel strategy for controlling aberrant T-cell trafficking, hence for the development of innovative anti-inflammatory therapeutics.—Norling, L. V., Sampaio, A. L. F., Cooper, D., Perretti, M. Inhibitory control of endothelial galectin-1 on in vitro and in vivo lymphocyte trafficking.

Key Words: small interfering RNA • homing • delayed-type hypersensitivity