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Enhanced Antitumor Immunity in Mice Deficient in CD69

AuthorsEsplugues, Enric; Sancho, David; Vega-Ramos, Javier; Martínez-Alonso, Carlos; Syrbe, Uta; Hamann, Alf; Engel, Pablo; Sánchez Madrid, Francisco; Lauzurica, Pilar
Issue DateMay-2003
PublisherRockefeller University Press
CitationThe Journal of Experimental Medicine, Volume 197, Number 9, May 5, 2003, pp. 1093–1106
AbstractWe 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.
DescriptionCopyright © by The Rockefeller University Press
Appears in Collections:(CNB) Artículos
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