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International Immunology Advance Access originally published online on December 20, 2007
International Immunology 2008 20(2):235-245; doi:10.1093/intimm/dxm134
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

LPS-activated monocytes suppress T-cell immune responses and induce FOXP3+ T cells through a COX-2–PGE2-dependent mechanism

Tone Bryn1,2,4,*, Sheraz Yaqub1,2,*, Milada Mahic1,2, Karen Henjum1,2,3, Einar M. Aandahl1,2 and Kjetil Taskén1,2

1 Biotechnology Centre of Oslo
2 Centre for Molecular Medicine Norway, Nordic EMBL Partnership, University of Oslo, N-0317 Oslo, Norway
3 Department of Gastroenterological Surgery, Ullevaal University Hospital, Oslo, Norway
4 Present address: AstraZeneca, Oslo, Norway

Correspondence to: K. Taskén; E-mail: kjetil.tasken{at}biotek.uio.no

Monocytes initiate innate immune responses and interact with T cells to induce antigen-specific immune responses by antigen presentation and secretion of humoral factors. We have previously shown that adaptive regulatory T cells inhibit T-cell effector functions in a cyclooxygenase (COX)-2–prostaglandin E2 (PGE2)-dependent manner and that PGE2 converts resting CD4+CD25– T cells into FOXP3+ T cells with a suppressive phenotype. Here, we demonstrate that stimulation of monocytes with LPS leads to suppression of T-cell immune responses by a COX-2–PGE2-dependent mechanism that is reversible with COX-2 inhibitors as well as PGE2-neutralizing antibody and cAMP antagonist. Furthermore, we show that LPS-activated monocytes induce FOXP3 expression in resting CD4+CD25– T cells by the same pathway. These results suggest that monocytes are able to efficiently suppress T-cell immune responses in a regulatory manner and elicit an inhibitory immune profile.

Keywords: COX-2, FOXP3, human, LPS, monocytes, PGE2

* These authors contributed equally to the study.

Transmitting editor: A. Falus

Received 25 April 2007, accepted 22 November 2007.


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