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dc.contributor.authorNombela-Arrieta, César-
dc.contributor.authorMempel, Thorsten R.-
dc.contributor.authorSoriano, Silvia F.-
dc.contributor.authorMazo, Irina-
dc.contributor.authorWymann, Matthias P.-
dc.contributor.authorHirsch, Emilio-
dc.contributor.authorMartínez-Alonso, Carlos-
dc.contributor.authorFukui, Yoshinori-
dc.contributor.authorAndrian, Ulrich H. von-
dc.contributor.authorStein, Jens V.-
dc.date.accessioned2008-03-18T09:55:46Z-
dc.date.available2008-03-18T09:55:46Z-
dc.date.issued2007-03-
dc.identifier.citationThe Journal of Experimental Medicine, Vol. 204, No. 3, March 19, 2007, pp. 497–510en_US
dc.identifier.isbn1540-9538-
dc.identifier.urihttp://hdl.handle.net/10261/3237-
dc.descriptionCopyright by The Rockefeller University Pressen_US
dc.description.abstractRecent observations using multiphoton intravital microscopy (MP-IVM) have uncovered an unexpectedly high lymphocyte motility within peripheral lymph nodes (PLNs). Lymphocyteexpressed intracellular signaling molecules governing interstitial movement remain largely unknown. Here, we used MP-IVM of murine PLNs to examine interstitial motility of lymphocytes lacking the Rac guanine exchange factor DOCK2 and phosphoinositide-3-kinase (PI3Kƴ), signaling molecules that act downstream of G protein–coupled receptors, including chemokine receptors (CKRs). T and B cells lacking DOCK2 alone or DOCK2 and PI3Kƴ displayed markedly reduced motility inside T cell area and B cell follicle, respectively. Lack of PI3Kƴ alone had no effect on migration velocity but resulted in increased turning angles of T cells. As lymphocyte egress from PLNs requires the sphingosine-1-phosphate (S1P) receptor 1, a Gi protein–coupled receptor similar to CKR, we further analyzed whether DOCK2 and PI3Kƴ contributed to S1P-triggered signaling events. S1P-induced cell migration was signifi cantly reduced in T and B cells lacking DOCK2, whereas T cell–expressed PI3Kƴ contributed to F-actin polymerization and protein kinase B phosphorylation but not migration. These fi ndings correlated with delayed lymphocyte egress from PLNs in the absence of DOCK2 but not PI3K, and a markedly reduced cell motility of DOCK2-defi cient T cells in close proximity to efferent lymphatic vessels. In summary, our data support a central role for DOCK2, and to a lesser extent T cell–expressed PI3Kƴ, for signal transduction during interstitial lymphocyte migration and S1P-mediated egress.en_US
dc.format.extent3186031 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherRockefeller University Pressen_US
dc.rightsopenAccessen_US
dc.subjectHematologyen_US
dc.titleA central role for DOCK2 during interstitial lymphocyte motility and sphingosine-1-phosphate–mediated egressen_US
dc.typeArtículoen_US
dc.identifier.doi10.1084/jem.20061780-
dc.description.peerreviewedPeer revieweden_US
Appears in Collections:(CNB) Artículos
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