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dc.contributor.authorAli, Amal J.
dc.contributor.authorAbuElela, Ayman
dc.contributor.authorMerzaban, Jasmeen
dc.date.accessioned2017-05-22T06:58:02Z
dc.date.available2017-05-22T06:58:02Z
dc.date.issued2017-05-03
dc.identifier.citationAli AJ, Abuelela AF, Merzaban JS (2017) An Analysis of Trafficking Receptors Shows that CD44 and P-Selectin Glycoprotein Ligand-1 Collectively Control the Migration of Activated Human T-Cells. Frontiers in Immunology 8. Available: http://dx.doi.org/10.3389/fimmu.2017.00492.
dc.identifier.issn1664-3224
dc.identifier.pmid28515724
dc.identifier.doi10.3389/fimmu.2017.00492
dc.identifier.urihttp://hdl.handle.net/10754/623673
dc.description.abstractSelectins guide the traffic of activated T-cells through the blood stream by mediating their tethering and rolling onto inflamed endothelium, in this way acting as beacons to help navigate them to sites of inflammation. Here, we present a comprehensive analysis of E-selectin ligands expressed on activated human T-cells. We identified several novel glycoproteins that function as E-selectin ligands. Specifically, we compared the role of P-selectin glycoprotein ligand-1 (PSGL-1) and CD43, known E-selectin ligands, to CD44, a ligand that has not previously been characterized as an E-selectin ligand on activated human T-cells. We showed that CD44 acts as a functional E-selectin ligand when expressed on both CD4+ and CD8+ T-cells. Moreover, the CD44 protein carries a binding epitope identifying it as hematopoietic cell E- and/or L-selectin ligand (HCELL). Furthermore, by knocking down these ligands individually or together in primary activated human T-cells, we demonstrated that CD44/HCELL, and not CD43, cooperates with PSGL-1 as a major E-selectin ligand. Additionally, we demonstrated the relevance of our findings to chronic autoimmune disease, by showing that CD44/HCELL and PSGL-1, but not CD43, from T-cells isolated from psoriasis patients, bind E-selectin.
dc.description.sponsorshipThis work was supported by the King Abdullah University of Science and Technology (KAUST) Faculty Baseline Research Funding Program as well as a Competitive Research Grant (CRG2_R2_13_MERZ_KAUST_1) to JM. The authors would like to thank Dr. Samir M. Hamdan for discussions regarding SPR studies and Ms. Samar A. Rostom for her support in the management of the lab. The authors would also like to thank Carolyn Unck from the Academic Writing Services at KAUST for editing the manuscript. In addition, a special thanks to Dr. Aswini K. Panigrahi from the Bioscience Core Lab facility for the mass spectrometry assistance and the rest of the members of the Cell Migration and Signaling Laboratory for their support.
dc.publisherFrontiers Media SA
dc.relation.urlhttp://journal.frontiersin.org/article/10.3389/fimmu.2017.00492/full
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectCell adhesion
dc.subjectE-selectin
dc.subjectPsoriasis
dc.subjectCD44
dc.subjectcell migration
dc.subjectP-selectin Glycoprotein Ligand-1 (Cd162)
dc.subjectHematopoietic Cell E- And/or L-selectin Ligand
dc.subjectHuman Activated T-cells
dc.titleAn Analysis of Trafficking Receptors Shows that CD44 and P-Selectin Glycoprotein Ligand-1 Collectively Control the Migration of Activated Human T-Cells
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.identifier.journalFrontiers in Immunology
dc.eprint.versionPublisher's Version/PDF
kaust.personAli, Amal J.
kaust.personAbuElela, Ayman
kaust.personMerzaban, Jasmeen S.
kaust.grant.numberCRG2_R2_13_MERZ_KAUST_1
refterms.dateFOA2018-06-13T17:32:07Z


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This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Except where otherwise noted, this item's license is described as This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.