| First Author | Temchura VV | Year | 2005 |
| Journal | Eur J Immunol | Volume | 35 |
| Issue | 9 | Pages | 2738-47 |
| PubMed ID | 16114106 | Mgi Jnum | J:113492 |
| Mgi Id | MGI:3686837 | Doi | 10.1002/eji.200425641 |
| Citation | Temchura VV, et al. (2005) Role of the aryl hydrocarbon receptor in thymocyte emigration in vivo. Eur J Immunol 35(9):2738-47 |
| abstractText | 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-TCRbeta-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. |
