CXCL12 Regulates through JAK1 and JAK2 Formation of Productive Immunological Synapses. [artículo]
Por: Criado Carrasco, Gabriel [Instituto de Investigación i+12] | Pablos Álvarez, José Luis [Reumatología].
Colaborador(es): Instituto de Investigación imas12 | Servicio de Reumatología.
Tipo de material: ArtículoEditor: Journal of immunology (Baltimore, Md. : 1950), 2015Descripción: 194(11):5509-19.Recursos en línea: Solicitar documento Resumen: The adaptive immune response requires interaction between T cells and APC to form a specialized structure termed the immune synapse (IS). Although the TCR is essential for IS organization, other factors such as chemokines participate in this process. In this study, we show that the chemokine CXCL12-mediated signaling contributes to correct IS organization and therefore influences T cell activation. CXCR4 downregulation or blockade on T cells caused defective actin polymerization at the contact site with APC, altered microtubule-organizing center polarization and the IS structure, and reduced T cell/APC contact duration. T cell activation was thus inhibited, as shown by reduced expression of CD25 and CD69 markers and of IL-2 mRNA levels. The results indicate that, through Gi and JAK1 and 2 kinases activation, CXCL12 signaling cooperates to build the IS and to maintain adhesive contacts between APC and T cells, required for continuous TCR signaling.Tipo de ítem | Ubicación actual | Signatura | Estado | Fecha de vencimiento |
---|---|---|---|---|
Artículo | PC16903 (Navegar estantería) | Disponible |
Navegando Hospital Universitario 12 de Octubre Estantes Cerrar el navegador de estanterías
Formato Vancouver:
Cascio G, Martín Cófreces NB, Rodríguez Frade JM, López Cotarelo P, Criado G, Pablos JL et al. CXCL12 Regulates through JAK1 and JAK2 Formation of Productive Immunological Synapses. J Immunol. 2015 Jun 1;194(11):5509-19.
PMID: 25917087
Contiene63 referencias
The adaptive immune response requires interaction between T cells and APC to form a specialized structure termed the immune synapse (IS). Although the TCR is essential for IS organization, other factors such as chemokines participate in this process. In this study, we show that the chemokine CXCL12-mediated signaling contributes to correct IS organization and therefore influences T cell activation. CXCR4 downregulation or blockade on T cells caused defective actin polymerization at the contact site with APC, altered microtubule-organizing center polarization and the IS structure, and reduced T cell/APC contact duration. T cell activation was thus inhibited, as shown by reduced expression of CD25 and CD69 markers and of IL-2 mRNA levels. The results indicate that, through Gi and JAK1 and 2 kinases activation, CXCL12 signaling cooperates to build the IS and to maintain adhesive contacts between APC and T cells, required for continuous TCR signaling.
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