Role of the aryl hydrocarbon receptor in thymocyte emigration in vivo

The aryl hydrocarbon receptor (AHR) is a ligand‐dependent member of the PAS‐bHLH‐family of nuclear receptors. Anthropogenic ligands include environmental contaminants such as 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD). Over‐activation of the AHR causes thymus atrophy and immunosuppression. Signaling...

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Bibliographic Details
Published in:European Journal of Immunology 2005-09, Vol.35 (9), p.2738-2747
Main Authors: Temchura, Vladimir V., Frericks, Markus, Nacken, Wolfgang, Esser, Charlotte
Format: Article
Language:English
Subjects:
Animals
Aryl hydrocarbon receptor
Calgranulin B - genetics
Calgranulin B - immunology
Cell Differentiation - immunology
Cell Movement - immunology
Emigration
Flow Cytometry
Gene Expression Profiling
Immunophenotyping
Mice
Mice, Inbred C57BL
Mice, Knockout
Microarray
Oligonucleotide Array Sequence Analysis
Polychlorinated Dibenzodioxins - pharmacology
Receptors, Aryl Hydrocarbon - immunology
RNA - chemistry
RNA - genetics
S100A9
Spleen - immunology
T-Lymphocytes - cytology
T-Lymphocytes - immunology
Thymus
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Summary:The aryl hydrocarbon receptor (AHR) is a ligand‐dependent member of the PAS‐bHLH‐family of nuclear receptors. Anthropogenic ligands include environmental contaminants such as 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD). Over‐activation of the AHR causes thymus atrophy and immunosuppression. Signaling via the AHR changes the thymocyte differentiation program at several checkpoints, in particular within the CD4–CD8– double‐negative (DN) thymocyte subset. Here, we show that AHR over‐activation led to the preferential emigration of DN thymocytes to the periphery and accumulation in the spleen. Some of these recent thymic emigrants (RTE) had a novel “activated immature” phenotype (CD3–TCRβ–CD25+/intCD44–CD45RB+/intCD62L+CD69– cells). Gene expression profiling of DN RTE revealed 15 genes that were up‐regulated more than threefold by TCDD, including the S100A9 gene. Exposure of S100A9 null mice to TCDD showed a role for this protein in AHR‐mediated thymic egress.
ISSN:0014-2980
1521-4141
1365-2567
DOI:10.1002/eji.200425641