Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on September 1, 2007

Published online before print June 27, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0307134


Received for publication March 2, 2007.
Revised May 18, 2007.
Accepted for publication May 31, 2007.


Article

CD4+ T lymphocyte subsets express connexin 43 and establish gap junction channel communication with macrophages in vitro

Alexandra Bermudez-Fajardo *, Minna Ylihärsilä *, W. Howard Evans {dagger}, Andrew C. Newby {ddagger}, and Ernesto Oviedo-Orta *@

*School of Biomedical and Molecular Sciences, University of Surrey, Guildford, United Kingdom; {dagger}Department of Medical Biochemistry and Immunology, Cardiff University School of Medicine, Wales, United Kingdom; and {ddagger}Bristol Heart Institute, Bristol Royal Infirmary, Bristol, United Kingdom

@ To whom correspondence should be addressed. E-mail: e.oviedo-orta{at}surrey.ac.uk.


   Abstract

Gap junction channels constructed of connexins (Cxs) are expressed by peripheral and secondary lymphoid organ-derived lymphocytes. These channels in the plasma membrane play key roles in a range of lymphocyte functions exemplified by the synthesis and secretion of Igs and cytokines and during transmigration across the endothelium. Most recently, their involvement in antigen cross-presentation has also been established. We report here for the first time the expression of mRNA and protein encoding Cx43 in mouse-derived CD4+ Th0, Th1, and Th2 lymphocyte subpopulations and demonstrate the establishment gap junction channel formation with primary macrophages in vitro. We show that this mode of direct communication is particularly favored in Th1-macrophage interactions and that LPS inhibits lymphocyte-macrophage cross-talk independently of the subset of lymphocyte involved. Our work suggests that gap junction-mediated communication can be modulated in the absence of specific antigenic stimulation. Therefore, a further mechanism featuring gap junction-mediated communication may be implicated in immune regulation.

Key Words: inflammation • intercellular • flow cytometry • lymphocytes







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Copyright © 2007 by the Society for Leukocyte Biology.