Skip Navigation



International Immunology Advance Access published online on June 20, 2005
International Immunology, doi:10.1093/intimm/dxh274
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
17/7/943    most recent
dxh274v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Walzer, T.
Right arrow Articles by De Smedt, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Walzer, T.
Right arrow Articles by De Smedt, T.
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
Received March 23, 2005
Accepted April 26, 2005

Article

Dendritic cell function in mice lacking Plexin C1

Thierry Walzer 1*, Laurent Galibert 1, and Thibaut De Smedt 2

1 Amgen Inc., Department of Immune Regulation, 1201 Amgen Court West Seattle, WA 98119, USA
2 Amgen Inc., Department of Immune Regulation, 1201 Amgen Court West Seattle, WA 98119, USA; Present address: Apoxis S.A., 18-20 Avenue de Sevelin, CH-1004 Lausanne, Switzerland

* To whom correspondence should be addressed.
Thierry Walzer, E-mail: twalzer2002{at}yahoo.fr


  Abstract

Semaphorins are secreted or transmembrane proteins that provide essential repulsive guidance cues to growing axons or endothelial cells through their receptors of the Plexin and Neuropilin family. Semaphorins and Plexins are also expressed in the immune system where their function remains elusive. In particular, Plexin C1 is expressed by mouse dendritic cells (DCs) and is the receptor for the poxvirus semaphorin homolog A39R. We previously found that Plexin C1 engagement by A39R inhibits integrin-mediated DC adhesion and chemokine-induced migration. Here, we show that a cellular ligand for Plexin C1 is expressed both by activated T cells and DCs, suggesting that Plexin C1 might be engaged on DCs both in cis and in trans. We used Plexin C1-/- mice to explore the role of Plexin C1 in DC function. DC development is unaffected in these mice. In two different in vivo assays, Plexin C1-/- DC migration to lymph nodes (LNs) was lower than that of wild-type (WT) DC but this difference was not statistically significant. Plexin C1-/- bone marrow-derived DCs induced normal in vitro T cell responses but reduced in vivo T cell responses when injected subcutaneously to WT mice. Finally, in vivo T cell responses to ovalbumin peptide and contact hypersensitivity to dinitrofluorobenzene were slightly decreased in Plexin C1 -/- mice. These results suggest a role for Plexin C1 in DC migration or mobility within the LNs.

Keywords: antigen presentation; guidance; motility; semaphorins; trafficking.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol. Endocrinol.Home page
C. Xu and C.-M. Fan
Allocation of Paraventricular and Supraoptic Neurons Requires Sim1 Function: A Role for a Sim1 Downstream Gene PlexinC1
Mol. Endocrinol., May 1, 2007; 21(5): 1234 - 1245.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
L. Rossi, R. Manfredini, F. Bertolini, D. Ferrari, M. Fogli, R. Zini, S. Salati, V. Salvestrini, S. Gulinelli, E. Adinolfi, et al.
The extracellular nucleotide UTP is a potent inducer of hematopoietic stem cell migration
Blood, January 15, 2007; 109(2): 533 - 542.
[Abstract] [Full Text] [PDF]


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.