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Blood, 1 August 2004, Vol. 104, No. 3, pp. 619-625.
Prepublished online as a Blood First Edition Paper on April 1, 2004; DOI 10.1182/blood-2003-11-3943.
 Previous Article | Table of Contents | Next Article 
CHEMOKINES
Chemokine receptor CCR7 induces intracellular signaling that inhibits apoptosis of mature dendritic cells
Noelia Sánchez-Sánchez,
Lorena Riol-Blanco,
Gonzalo de la Rosa,
Amaya Puig-Kröger,
Julio García-Bordas,
Daniel Martín,
Natividad Longo,
Antonio Cuadrado,
Carlos Cabañas,
Angel L. Corbí,
Paloma Sánchez-Mateos, and
José Luis Rodríguez-Fernández
From the Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid; Laboratorio de Inmunología, Hospital General Universitario Gregorio Marañón, Madrid; Departamento de Bioquímica and Instituto de Investigaciones Biomédicas Alberto Sols, Facultad de Medicina, Universidad Autónoma de Madrid; and Instituto de Farmacología y Toxicología Consejo Superior de Investigaciones Científicas (CSIC)–Universidad Complutense de Madrid (UCM), Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Acquisition of CCR7 expression is an important phenotype change during dendritic cell (DC) maturation that endows these cells with the capability to migrate to lymph nodes. We have analyzed the possible role of CCR7 on the regulation of the survival of DCs. Stimulation with CCR7 ligands CCL19 and CCL21 inhibits apoptotic hallmarks of serum-deprived DCs, including membrane phosphatidylserine exposure, loss of mitochondria membrane potential, increased membrane blebs, and nuclear changes. Both chemokines induced a rapid activation of phosphatidylinositol 3'-kinase/Akt1 (PI3K/Akt1), with a prolonged and persistent activation of Akt1. Interference with PI3K, Gi, or G protein   subunits abrogated the effects of the chemokines on Akt1 activation and on survival. In contrast, inhibition of extracellular signal-related kinase 1/2 (Erk1/2), p38, or c-Jun N-terminal kinase (JNK) was ineffective. Nuclear factor– B (NFB) was involved in the antiapoptotic effects of chemokines because inhibition of NFB blunted the effects of CCL19 and CCL21 on survival. Furthermore, chemokines induced down-regulation of the NFB inhibitor IB, an increase of NFB DNA-binding capability, and translocation of the NFB subunit p65 to the nucleus. In summary, in addition to its well-established role in chemotaxis, we show that CCR7 also induces antiapoptotic signaling in mature DCs.
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