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dc.creatorEsplugues, Enric-
dc.creatorSancho, David-
dc.creatorVega-Ramos, Javier-
dc.creatorMartínez-Alonso, Carlos-
dc.creatorSyrbe, Uta-
dc.creatorHamann, Alf-
dc.creatorEngel, Pablo-
dc.creatorSánchez Madrid, Francisco-
dc.creatorLauzurica, Pilar-
dc.date2008-03-25T07:56:32Z-
dc.date2008-03-25T07:56:32Z-
dc.date2003-05-
dc.date.accessioned2017-01-31T01:00:53Z-
dc.date.available2017-01-31T01:00:53Z-
dc.identifierThe Journal of Experimental Medicine, Volume 197, Number 9, May 5, 2003, pp. 1093–1106-
dc.identifier0022-1007-
dc.identifierhttp://hdl.handle.net/10261/3282-
dc.identifier10.1084/jem.20021337-
dc.identifier.urihttp://dspace.mediu.edu.my:8181/xmlui/handle/10261/3282-
dc.descriptionCopyright © by The Rockefeller University Press-
dc.descriptionWe 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.-
dc.descriptionPeer reviewed-
dc.format263366 bytes-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherRockefeller University Press-
dc.rightsopenAccess-
dc.subjectCytokines-
dc.subjectHomeostasis-
dc.subjectApoptosis-
dc.titleEnhanced Antitumor Immunity in Mice Deficient in CD69-
dc.typeArtículo-
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