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Prepublished online as a Blood First Edition Paper on May 29, 2003; DOI 10.1182/blood-2003-02-0637.
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Blood, 15 September 2003, Vol. 102, No. 6, pp. 2173-2179
IMMUNOBIOLOGY
Anergic T cells exert antigen-independent inhibition of cell-cell interactions via chemokine metabolism
Martha J. James,
Lavina Belaramani,
Kanella Prodromidou,
Arpita Datta,
Sussan Nourshargh,
Giovanna Lombardi,
Julian Dyson,
Diane Scott,
Elizabeth Simpson,
Lorraine Cardozo,
Anthony Warrens,
Richard M. Szydlo,
Robert I. Lechler, and
Federica M. Marelli-Berg
From the Department of Immunology, Faculty of Medicine, Cardiovascular Medicine Unit, Transplantation Biology, Medical Research Council Clinical Research Centre; and Department of Hematology, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Due to their ability to inhibit antigen-induced T-cell activation in vitro and in vivo, anergic T cells can be considered part of the spectrum of immunoregulatory T lymphocytes. Here we report that both murine and human anergic T cells can impair the ability of parenchymal cells (including endothelial and epithelial cells) to establish cell-cell interactions necessary to sustain leukocyte migration in vitro and tissue infiltration in vivo. The inhibition is reversible and cell-contact dependent but does not require cognate recognition of the parenchymal cells to occur. Instrumental to this effect is the increased cell surface expression and enzymatic activity of molecules such as CD26 (dipeptidyl-peptidase IV), which may act by metabolizing chemoattractants bound to the endothelial/epithelial cell surface. These results describe a previously unknown antigen-independent anti-inflammatory activity by locally generated anergic T cells and define a novel mechanism for the long-known immunoregulatory properties of these cells.
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