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Vol. 302, Issue 1, 290-295, July 2002

Low-Molecular-Weight Heparins Inhibit CCL21-Induced T Cell Adhesion and Migration

Kent W. Christopherson, II, James J. Campbell, Jeffrey B. Travers and Robert A. Hromas

Departments of (K.W.C., R.A.H)Biochemistry/Molecular Biology and Hematology/Oncology, and Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana; (J.J.C.)Joint Program in Transfusion Medicine, Children's Hospital, and Department of Pathology, Harvard Medical School, Boston, Massachusetts; and (J.B.T)Department of Dermatology, Wells Center for Pediatric Research, and Riley Hospital for Children, Indianapolis, Indiana

The chemokine CCL21, also known as Exodus-2/6-Ckine/secondary lymphoid-tissue chemokine/T cell activator protein-4, is the most potent stimulator of T cell migration and adhesion yet described. Endothelial heparin-like glycosaminoglycans (GAGs) are thought to present chemokines at sites of inflammation, maintaining a local concentration gradient to which leukocytes can respond. In contrast, this study found that GAGs markedly inhibit the ability of CCL21 to stimulate T cell adhesion and chemotaxis. Enzymes, such as heparinase, that split GAGs into component-sulfated saccharides abrogate this inhibition, suggesting a mechanism for local tissue regulation of CCL21 function. Low-molecular-weight heparins also strongly inhibit CCL21 adhesion and chemotaxis. Therefore, low-molecular-weight heparins may be effective therapeutic agents in decreasing the pathology of T cell-infiltrative autoimmune diseases by targeting the CCL21 regulation of T cell infiltration.

0022-3565/02/3021-0290$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2002 by The American Society for Pharmacology and Experimental Therapeutics


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