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CCL2 Inhibits the Apoptosis Program Induced by Growth Factor Deprivation, Rescuing Functional T Cells¹

Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid, Spain

The precise mechanisms involved in the switch between the clonal expansion and contraction phases of a CD8⁺ T cell response remain to be fully elucidated. One of the mechanisms implicated in the contraction phase is cytokine deprivation, which triggers apoptosis in these cells. CCR2 chemokine receptor is up-regulated following IL-2 deprivation, and its ligand CCL2 plays an essential role preventing apoptosis induced by IL-2 withdrawal not only in CTLL2 cells, but also in mouse Ag-activated primary CD8⁺ T cells because it rescued functional CD8⁺ T cells from deprivation induced apoptosis, promoting proliferation in response to subsequent addition of IL-2 or to secondary antigenic challenges. Thus, up-regulation of the CCR2 upon growth factor withdrawal together with the protective effects of CCL2, represent a double-edged survival strategy, protecting cells from apoptosis and enabling them to migrate toward sites where Ag and/or growth factors are available.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants SAF2003-00519 and SAF2006-04903 (to J.A.G.-S.) and SAF2006–4826 (to A.S.) from Spanish Ministry of Education and Science contracts.

² E.D.-G., R.V., and M.J. del P. contributed equally to this work and should be considered as joint first authors.

³ Address correspondence and reprint requests to Dr. Jose A. Garcia-Sanz, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Ramiro de Maeztu 9, 28040 Madrid, Spain. E-mail address: jasanz{at}cib.csic.es

⁴ Abbreviation used in this paper: PI, propidium iodide.

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