Down-Modulation of CXCR3 Surface Expression and Function in CD8 super(+) T Cells from Cutaneous T Cell Lymphoma Patients

Viruses can escape destruction by the immune system by exploitation of the chemokine-chemokine receptor system. It is less established whether human cancers can adopt similar strategies to evade immunologic control. In this study, we show that advanced cutaneous T cell lymphoma (CTCL) is associated...

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Bibliographic Details
Published in:Journal of Immunology 2007-09, Vol.179 (6), p.4272-4282
Main Authors: Winter, Dorian, Moser, Julia, Kriehuber, Ernst, Wiesner, Christoph, Knobler, Robert, Trautinger, Franz, Bombosi, Paula, Stingl, Georg, Petzelbauer, Peter, Rot, Antal, Maurer, Dieter
Format: Article
Language:English
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Summary:Viruses can escape destruction by the immune system by exploitation of the chemokine-chemokine receptor system. It is less established whether human cancers can adopt similar strategies to evade immunologic control. In this study, we show that advanced cutaneous T cell lymphoma (CTCL) is associated with selective and efficient inactivation of CXCR3-dependent T cell migration. Our studies demonstrate that this alteration is at least in part due to CXCR3 down-regulation in vivo by elevated serum levels of CXCR3 ligands. The T cell population most affected by this down-regulatory mechanism are CD8 super(+) cytotoxic effector T cells. In CTCL patients, cytotoxic effector T cells have strongly reduced surface CXCR3 expression, accumulate in peripheral blood, but are virtually absent from CTCL tumor lesions, indicating an inability to extravasate into lymphoma tissue. CTCL-associated inactivation of effector cell recruitment may be a paradigmatic example of a new type of immune escape mechanisms shielding the neoplasm from a tumoricidal attack.
ISSN:0022-1767
1365-2567