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Published online before print March 14, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1106710

Received for publication November 30, 2006.
Revised February 23, 2007.
Accepted for publication February 26, 2007.

Article

Leukocyte membrane "expansion": a central mechanism for leukocyte extravasation

Neutrophil Signalling Group, School of Medicine, Cardiff University, Cardiff, United Kingdom

^@ To whom correspondence should be addressed. E-mail: hallettmb{at}cf.ac.uk.

	Abstract

The infiltration of inflamed tissues by leukocytes is a key event in the development and progression of inflammation. Although individual cytokines, which coordinate extravasation, have become the targets for therapy, a mechanism that is common to white cell extravasation, regardless of the specific molecular mechanism involved, would represent a more attractive therapeutic target. Such a target may be represented by the events underlying the spreading of leukocytes on the endothelium, which is a necessary prelude to extravasation. This leukocyte "spreading" involves an apparent increase in the cell surface area. The aim of this review is to examine whether the mechanism underlying the apparent expansion of plasma membrane surface area during leukocyte extravasation could be an "Achilles’ heel," which is amenable to therapeutic intervention. In this short review, we evaluate the models proposed for the mechanism of membrane "expansion" and discuss recent data, which point to a mechanism of membrane "unwrinkling." The molecular pathway for the unwrinkling of the leukocyte plasma membrane may involve Ca²⁺ activation of µ-calpain and cleavage of cytoskeletal linkage molecules such as talin and ezrin. This route could be common to all extravasation signals and thus, represents a potential target for anti-inflammatory therapy.

Key Words: adhesion • neutrophil • calcium

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