Miltenyi Biotec GmbH
Originally published online as doi:10.1189/jlb.0508280 on October 1, 2009

Published online before print October 1, 2009
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Buy
Right arrow All Versions of this Article:
jlb.0508280v1
87/2/193    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 Biburger, M.
Right arrow Articles by Tiegs, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Biburger, M.
Right arrow Articles by Tiegs, G.
Related Collections
Right arrowRelated Article
(Journal of Leukocyte Biology. 2010;87:193-202.)
© 2010 Society for Leukocyte Biology

Pivotal Advance: Heme oxygenase 1 expression by human CD4+ T cells is not sufficient for their development of immunoregulatory capacity

Markus Biburger*,{dagger},1, Gabi Theiner{ddagger},1, Mirjam Schädle{dagger}, Gerold Schuler{ddagger} and Gisa Tiegs{dagger},§,2

* Nikolaus Fiebiger Center for Molecular Medicine, Medical Department III, and
{ddagger} Department of Dermatology, University Hospital of Erlangen, Germany;
{dagger} Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nuremberg, Germany; and
§ Division of Experimental Immunology and Hepatology, Center of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

2. Correspondence: Division of Experimental Immunology and Hepatology, University Medical Centre Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany. E-mail: g.tiegs{at}uke.de

ABSTRACT

HO-1 is the only inducible one of three isoenzymes that catalyzes the oxidative degradation of heme. HO-1 is inducible by various cellular stress factors and exerts cytoprotective and immunomodulatory effects. Recent publications demonstrated that HO-1 is constitutively expressed by CD4+CD25+ Tregs and induced in CD4+CD25– T cells upon FoxP3 transfection. Here, we investigated whether HO-1 was essential and sufficient for human Tregs to exert immunosuppression in vitro. PGJ2 induced pronounced expression of HO-1 in CD4+CD25– T cells without accompanying FoxP3 induction. Treatment of CD4+CD25– T cells with PGJ2 decreased their proliferation, whereas the HO-1 inhibitor SnPP enhanced the proliferation of HO-1-expressing Tregs, suggesting that HO-1 may modulate the proliferative capacity of T lymphocytes. HO-1 modulation by SnPP treatment of Tregs or PGJ2 treatment of CD4+CD25– T cells neither suppressed nor induced immune-modulatory function in these cells, respectively, as measured by responder-cell proliferation and/or IL-2 production. In summary, these data suggest that HO-1 expression by Tregs might contribute to their typical reluctance to proliferate but does not account independently for their suppressive functions.

Key Words: tolerance • regulatory T cells • immune modulation • CD4+CD25+ Tregs • proliferation


Related Article

Editorial: Heme oxygenase-1 and dendritic cells: what else?
Philippe Blancou and Ignacio Anegon
J. Leukoc. Biol. 2010 87: 185-187. [Full Text] [PDF]