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Functional Inactivation of CXC Chemokine Receptor 4–mediated Responses through SOCS3 Up-regulation

AutorSoriano, Silvia F.; Hernanz-Falcón, Patricia; Rodríguez Frade, José M.; Martín de Ana, Ana; Garzón, Ruth; Carvalho-Pinto, Carla E.; Vila-Coro, Antonio J.; Zaballos, Ángel; Balomenos, Dimitrios ; Martínez-Alonso, Carlos; Mellado, Mario
Palabras claveSOCS3
JAK-STAT activation
Chemokine signaling
Cytokine signaling
Fecha de publicaciónago-2002
EditorRockefeller University Press
CitaciónThe Journal of Experimental Medicine, Volume 196, Number 3, August 5, 2002, pp. 311–321
ResumenHematopoietic cell growth, differentiation, and chemotactic responses require coordinated action between cytokines and chemokines. Cytokines promote receptor oligomerization, followed by Janus kinase (JAK) kinase activation, signal transducers and transactivators of transcription (STAT) nuclear translocation, and transcription of cytokine-responsive genes. These include genes that encode a family of negative regulators of cytokine signaling, the suppressors of cytokine signaling (SOCS) proteins. After binding their specific receptors, chemokines trigger receptor dimerization and activate the JAK/STAT pathway. We show that SOCS3 overexpression or up-regulation, stimulated by a cytokine such as growth hormone, impairs the response to CXCL12, measured by Ca2+ flux and chemotaxis in vitro and in vivo. This effect is mediated by SOCS3 binding to the CXC chemokine receptor 4 receptor, blocking JAK/STAT and G i pathways, without interfering with cell surface chemokine receptor expression. The data provide clear evidence for signaling cross-talk between cytokine and chemokine responses in building a functional immune system.
DescripciónCopyright pertenece a The Rockefeller University Press
URIhttp://hdl.handle.net/10261/3276
DOI10.1084/jem.20012041
ISSN0022-1007
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