Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on June 1, 2008

Published online before print March 27, 2008
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0607421v1
83/6/1423    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lauterbach, M.
Right arrow Articles by Mayadas, T. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lauterbach, M.
Right arrow Articles by Mayadas, T. N.
© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0607421

Received for publication June 21, 2007.
Revised February 19, 2008.
Accepted for publication February 20, 2008.

Article

Role of TNF priming and adhesion molecules in neutrophil recruitment to intravascular immune complexes

Michael Lauterbach , Peter O’Donnell , Kenichi Asano , and Tanya N. Mayadas @

Center of Excellence in Vascular Biology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA

@ To whom correspondence should be addressed. E-mail: tmayadas{at}rics.bwh.harvard.edu.


  Abstract

Neutrophils play an important role in immune complex (IC)-mediated diseases, but the mechanisms underlying their recruitment to sites of IC deposition remain largely undefined. Furthermore, neutrophils encounter cytokines that prime their effector functions, yet the physiological relevance of priming to neutrophil functions is unclear. Here, we demonstrate that TNF treatment of neutrophils ex vivo significantly increased their adhesion in a model of intravascularly deposited ICs in the cremaster muscle that is amenable to intravital microscopy, and this was not observed in the absence of ICs. Analyses of relevant knockout mice and neutrophil reconstitution revealed a critical role for Fc{gamma}Rs and membrane-activated complex 1 (Mac-1) in IC-mediated neutrophil adhesion. Furthermore, ICAM-1, a major Mac-1 ligand constitutively expressed on unactivated endothelium, significantly contributed to this process. These data suggest that TNF priming promotes Fc{gamma}R interaction with intravascular ICs, leading to the binding of Mac-1 to ICAM-1 and subsequent neutrophil arrest.

Key Words: adhesion molecules • Fc receptors • cytokines • cell trafficking






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2008 by the Society for Leukocyte Biology.