2024-03-28T08:52:33Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/32822021-12-27T15:33:56Zcom_10261_25com_10261_1col_10261_278
Esplugues, Enric
Sancho, David
Vega-Ramos, Javier
Martínez-Alonso, Carlos
Syrbe, Uta
Hamann, Alf
Engel, Pablo
Sánchez Madrid, Francisco
Lauzurica, Pilar
2008-03-25T07:56:32Z
2008-03-25T07:56:32Z
2003-05
The Journal of Experimental Medicine, Volume 197, Number 9, May 5, 2003, pp. 1093–1106
0022-1007
http://hdl.handle.net/10261/3282
10.1084/jem.20021337
12732655
We 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.
eng
openAccess
Cytokines
Homeostasis
Apoptosis
Enhanced Antitumor Immunity in Mice Deficient in CD69
artículo