1. DSpace at MEDIU
  2. Harvested articles مقالات مستوردة من مؤسسات وجامعات عالمية
  3. Digital Csic
Please use this identifier to cite or link to this item: http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3237
Full metadata record
DC FieldValueLanguage
dc.creatorNombela-Arrieta, César-
dc.creatorMempel, Thorsten R.-
dc.creatorSoriano, Silvia F.-
dc.creatorMazo, Irina-
dc.creatorWymann, Matthias P.-
dc.creatorHirsch, Emilio-
dc.creatorMartínez-Alonso, Carlos-
dc.creatorFukui, Yoshinori-
dc.creatorAndrian, Ulrich H. von-
dc.creatorStein, Jens V.-
dc.date2008-03-18T09:55:46Z-
dc.date2008-03-18T09:55:46Z-
dc.date2007-03-
dc.date.accessioned2017-01-31T01:00:46Z-
dc.date.available2017-01-31T01:00:46Z-
dc.identifierThe Journal of Experimental Medicine, Vol. 204, No. 3, March 19, 2007, pp. 497–510-
dc.identifier1540-9538-
dc.identifierhttp://hdl.handle.net/10261/3237-
dc.identifier10.1084/jem.20061780-
dc.identifier.urihttp://dspace.mediu.edu.my:8181/xmlui/handle/10261/3237-
dc.descriptionCopyright by The Rockefeller University Press-
dc.descriptionRecent 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.-
dc.descriptionPeer reviewed-
dc.format3186031 bytes-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherRockefeller University Press-
dc.rightsopenAccess-
dc.subjectHematology-
dc.titleA central role for DOCK2 during interstitial lymphocyte motility and sphingosine-1-phosphate–mediated egress-
dc.typeArtículo-
Appears in Collections:Digital Csic

Files in This Item:
There are no files associated with this item.
Show simple item record


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.