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Blood, 1 December 2002, Vol. 100, No. 12, pp. 3853-3860
REVIEW ARTICLE
Leukocyte extravasation: chemokine transport and presentation
by the endothelium
Jim Middleton,
Angela M. Patterson,
Lucy Gardner,
Caroline Schmutz, and
Brian A. Ashton
From the Leopold Muller Arthritis Research Centre,
Centre for Science and Technology in Medicine, Keele University at
Robert Jones and Agnes Hunt Orthopaedic Hospital, Oswestry,
United Kingdom.
At sites of inflammation and in normal immune surveillance,
chemokines direct leukocyte migration across the endothelium. Many cell
types that are extravascular can produce chemokines, and for these
mediators to directly elicit leukocyte migration from the blood, they
would need to reach the luminal surface of the endothelium. This
article reviews the evidence that endothelial cells are active in
transcytosing chemokines to their luminal surfaces, where they are
presented to leukocytes. The endothelial binding sites that transport
and present chemokines include glycosaminoglycans (GAGs) and possibly
the Duffy antigen/receptor for chemokines (DARC). The binding residues
on chemokines that interact with GAGs are discussed, as are the
carbohydrate structures on GAGs that bind these cytokines. The
expression of particular GAG structures by endothelial cells may lend
selectivity to the type of chemokine presented in a given tissue,
thereby contributing to selective leukocyte recruitment. At the luminal
surface of the endothelium, chemokines are preferentially presented to
blood leukocytes on the tips of microvillous processes. Similarly,
certain adhesion molecules and chemokine receptors are also
preferentially distributed on leukocyte and endothelial microvilli, and
evidence suggests an important role for these structures in creating
the necessary surface topography for leukocyte migration. Finally, the
mechanisms of chemokine transcytosis and presentation by endothelial
cells are incorporated into the current model of chemokine-driven
leukocyte extravasation.
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