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Associated with Extracellular Matrix Fibronectin Provides a Stop Signal for Chemotactically Migrating T Cells1
*
Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel; and
Department of Internal Medicine, Meir Hospital, Kfar-Saba, Israel
The migration of T cells into extravascular sites of inflammation
is regulated by information derived from the molecular structure of the
invaded tissue and from chemokine and cytokine gradients in the context
of the extracellular matrix (ECM). Although recent studies have
highlighted the role of particular chemoattractants in leukocyte
migration, to date little is known about how specific combinations of
contextual signals control the migration of leukocytes and their
localization at sites of inflammation. Here we studied the interplay
between a pleiotropic cytokine, TNF-
, and two prototypic
chemoattractants, RANTES and stromal cell-derived factor-1
(SDF-1), on human CD45RO+ T cells migrating within an
ECM-like context. For this purpose, we used a newly constructed
three-dimensional gel system designed to follow, in real time, the
migration of individual leukocytes along chemotactic gradients in
vitro. We found that TNF-, which binds the ECM protein fibronectin
and lacks adhesion- and migration-promoting effects of its own, can act
as a proadhesive cytokine on T cells exposed to RANTES and SDF-1.
Furthermore, fibronectin-complexed TNF- provided anchorage signals
to the T cells as they moved directionally along chemoattractive
gradients. This effect of TNF- required an intact TNF- receptor
II subtype on the migrating T cells. The anchoring effect of TNF-
appears to be specific; IL-2, an integrin-activating proadhesive
cytokine, does not transmit stoppage signals to T cell migration
induced by RANTES. Thus, TNF- present in the ECM at sites of
inflammation may function to anchor T cells recruited to these sites by
chemotactic signals.
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