Microangiectasias: Structural regulators of lymphocyte transmigration
- Timothy W. Secomb*,
- Moritz A. Konerding†,
- Charles A. West‡,
- Mei Su‡,
- Alan J. Young‡, and
- Steven J. Mentzer‡,§
- *Department of Physiology, University of Arizona, Tucson, AZ 85724; †Department of Anatomy, Johannes Gutenberg University, D-55099 Mainz, Germany; and ‡Laboratory of Immunophysiology, Dana–Farber Cancer Institute, Harvard Surgical Research Laboratories, Harvard Medical School, Boston, MA 02115
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Communicated by Joseph E. Murray, Harvard Medical School, Boston, MA, April 14, 2003 (received for review March 7, 2003)
Abstract
The migration of lymphocytes into inflammatory tissue requires the migrating cell to overcome mechanical forces produced by blood flow. A generally accepted hypothesis is that these forces are overcome by a multistep sequence of adhesive interactions between lymphocytes and endothelial cells. This hypothesis has been recently challenged by results demonstrating wall shear stress on the order of 20 dyn/cm2 in vivo and infrequent lymphocyte–endothelial adhesion at wall shear stress >1–2 dyn/cm2 in vitro. Here, we show that lymphocyte slowing and transmigration in the skin is associated with microangiectasias, i.e., focal structural dilatations of microvessel segments. Microangiectasias are inducible within 4 days of the onset of inflammation and lead to a greater than 10-fold local reduction in wall shear stress. These findings support the hypothesis that a preparatory step to lymphocyte transmigration involves structural adaptations in the inflammatory microcirculation.
Footnotes
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↵ § To whom correspondence should be addressed at: G08 JFB, Dana–Farber Cancer Institute, 44 Binney Street, Boston, MA 02115. E-mail: smentzer{at}partners.org.
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Abbreviation: SEM, scanning electron microscopy.
- Copyright © 2003, The National Academy of Sciences
