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Enhanced Antitumor Immunity in Mice Deficient in CD69

AutorEsplugues, Enric; Sancho, David; Vega-Ramos, Javier; Martínez-Alonso, Carlos; Syrbe, Uta; Hamann, Alf; Engel, Pablo; Sánchez Madrid, Francisco; Lauzurica, Pilar
Palabras claveCytokines
Homeostasis
Apoptosis
Fecha de publicaciónmay-2003
EditorRockefeller University Press
CitaciónThe Journal of Experimental Medicine, Volume 197, Number 9, May 5, 2003, pp. 1093–1106
ResumenWe investigated the in vivo role of CD69 by analyzing the susceptibility of CD69 / mice to tumors. CD69 / mice challenged with MHC class I tumors (RMA-S and RM-1) showed greatly reduced tumor growth and prolonged survival compared with wild-type (WT) mice. The enhanced anti–tumor response was NK cell and T lymphocyte–mediated, and was due, at least in part, to an increase in local lymphocytes. Resistance of CD69 / mice to MHC class I tumor growth was also associated with increased production of the chemokine MCP-1, diminished TGF- production, and decreased lymphocyte apoptosis. Moreover, the in vivo blockade of TGF- in WT mice resulted in enhanced anti–tumor response. In addition, CD69 engagement induced NK and T cell production of TGF- , directly linking CD69 signaling to TGF- regulation. Furthermore, anti-CD69 antibody treatment in WT mice induced a specific down-regulation in CD69 expression that resulted in augmented anti–tumor response. These data unmask a novel role for CD69 as a negative regulator of anti–tumor responses and show the possibility of a novel approach for the therapy of tumors.
DescripciónCopyright © by The Rockefeller University Press
URIhttp://hdl.handle.net/10261/3282
DOI10.1084/jem.20021337
ISBN0022-1007
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