Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0108046 on December 26, 2008

Published online before print December 26, 2008
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Buy
Right arrow All Versions of this Article:
jlb.0108046v1
85/3/452    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 Jeffe, F.
Right arrow Articles by Wedemeyer, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jeffe, F.
Right arrow Articles by Wedemeyer, H.
(Journal of Leukocyte Biology. 2009;85:452-461.)
© 2009 by Society for Leukocyte Biology

Adenosine and IFN-{alpha} synergistically increase IFN-{gamma} production of human NK cells

Florian Jeffe1, Kerstin A. Stegmann1, Felix Broelsch, Michael P. Manns, Markus Cornberg and Heiner Wedemeyer2

Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany

2 Correspondence: Abteilung für Gastroenterologie, Hepatologie und Endokrinologie, Medizinische Hochschule Hannover, Carl Neuberg-Str.1, 30625 Hannover, Germany. E-mail: wedemeyer.heiner{at}mh-hannover.de

Prevention of overwhelming immune reactions is essential for an organism to survive. Adenosine, a ribonucleoside produced by various cell types during inflammatory processes, has been shown to inhibit effector functions of different immune cells. Here, we show that the adenosine A3 receptor agonist iodobenzyl methylcarboxamidoadenosine potently inhibited proliferation, IFN-{gamma} production, and cytotoxicity of activated human lymphoid cells. Stimulation of the A3 receptor also caused apoptosis of activated PBMC. However, when PBMC were stimulated with IFN-{alpha}, adenosine did not decrease, but synergistically increased, the IFN-{gamma} production of NK cells. This effect was also mediated mainly via the A3 receptor. Thus, our data suggest that adenosine differentially contributes to the regulation of immune responses during inflammatory processes: It may increase effector functions of NK cells in combination with IFN-{alpha} but also prevents overwhelming immune responses by inhibiting proliferation and induction of apoptosis of activated lymphoid cells. Future studies need to define the role of the different adenosine receptors in more detail.

Key Words: IB-Meca • A3 receptor