Skip Navigation


International Immunology Advance Access originally published online on March 4, 2005
International Immunology 2005 17(4):449-458; doi:10.1093/intimm/dxh225
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/4/449    most recent
dxh225v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fanning, A.
Right arrow Articles by Long, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fanning, A.
Right arrow Articles by Long, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

CD44 cross-linking induces protein kinase C-regulated migration of human T lymphocytes

Áine Fanning1, Yuri Volkov1, Michael Freeley2, Dermot Kelleher1,* and Aideen Long2,*

1 Department of Clinical Medicine, Trinity College, and Dublin Molecular Medicine Centre, James's Street, Dublin 8, Ireland
2 Department of Biochemistry, Royal College of Surgeons of Ireland, Dublin 2, Ireland

Correspondence to: Y. Volkov; E-mail: yvolkov{at}tcd.ie

The cell surface receptor CD44 is widely implicated in leukocyte migration to inflammatory sites. In this study, the responses of human T cells following cross-linking of CD44 were examined. We demonstrate that engagement of CD44 using immobilized mAbs or hyaluronan-enriched extracellular matrix lattices induces active migration in T lymphocytes accompanied by cycles of cytoskeletal rearrangement and cell polarization. We have investigated the functional impact and subcellular localization of protein kinase C (PKC) isoenzymes, ß and {delta}, previously shown by our group to be involved in active T cell locomotion induced by leukocyte function-associated antigen-1 (LFA-1) integrin receptors. PKCß was associated with the centrosome and the microtubule-rich tail of the polarized cell and PKC{delta} was predominantly located about the region of the microtubule organizing center. A selective pharmacological inhibitor of classical PKC isoforms, Gö6976, suppressed lymphocyte polarization and migration following CD44 ligation. Selective targeting of PKC{delta} using the pharmacological inhibitor rottlerin or a pseudosubstrate-blocking peptide reduced CD44-activated cell migration but did not completely ablate it. Our data demonstrate that ligation of CD44 induces phenotypic changes, cytoskeletal rearrangements and redistribution of PKC isoforms ß and {delta}, resulting in cell migration, as previously described for the cell surface receptor, LFA-1. This suggests potential convergence of intracellular signaling pathways induced via CD44 and LFA-1 integrin.

Keywords: microtubules, protein kinase C, T cell

* These authors contributed equally to this work.

Transmitting editor: A. Falus


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.