FOXP3+CD4+CD25+ Adaptive Regulatory T Cells Express Cyclooxygenase-2 and Suppress Effector T Cells by a Prostaglandin E2-Dependent Mechanism

CD4+CD25+ regulatory T (T(R)) cells suppress effector T cells by partly unknown mechanisms. In this study, we describe a population of human suppressive CD4+CD25+ adaptive T(R) (T(R)(adapt)) cells induced in vitro that express cyclooxygenase 2 (COX-2) and the transcription factor FOXP3. T(R)(adapt)...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2006-07, Vol.177 (1), p.246-254
Main Authors: Mahic, Milada, Yaqub, Sheraz, Johansson, C. Christian, Tasken, Kjetil, Aandahl, Einar M
Format: Article
Language:English
Subjects:
Cell Communication - immunology
Cells, Cultured
Cyclic AMP - biosynthesis
Cyclooxygenase 2 - biosynthesis
Cyclooxygenase 2 Inhibitors - pharmacology
Dinoprostone - antagonists & inhibitors
Dinoprostone - biosynthesis
Dinoprostone - metabolism
Dinoprostone - physiology
Enterotoxins - pharmacology
Forkhead Transcription Factors - biosynthesis
Forkhead Transcription Factors - physiology
Humans
Immunity, Innate
Immunosuppressive Agents - antagonists & inhibitors
Immunosuppressive Agents - pharmacology
Lymphocyte Activation - immunology
Prostaglandin Antagonists - physiology
Receptors, Interleukin-2 - biosynthesis
Receptors, Prostaglandin E - antagonists & inhibitors
T-Lymphocyte Subsets - enzymology
T-Lymphocyte Subsets - immunology
T-Lymphocyte Subsets - metabolism
T-Lymphocyte Subsets - microbiology
T-Lymphocytes, Regulatory - enzymology
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
T-Lymphocytes, Regulatory - microbiology
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Summary:CD4+CD25+ regulatory T (T(R)) cells suppress effector T cells by partly unknown mechanisms. In this study, we describe a population of human suppressive CD4+CD25+ adaptive T(R) (T(R)(adapt)) cells induced in vitro that express cyclooxygenase 2 (COX-2) and the transcription factor FOXP3. T(R)(adapt) cells produce PGE(2) and suppress effector T cell responses in a manner that is reversed by COX inhibitors and PGE(2) receptor-specific antagonists. In resting CD4+CD25- T cells, treatment with PGE(2) induced FOXP3 expression. Thus, autocrine and paracrine effects of PGE(2) produced by COX-2-positive T(R)(adapt) cells may be responsible for both the FOXP3+ phenotype and the mechanism used by these cells to suppress effector T cells.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.177.1.246