Targeted deletion of the aryl hydrocarbon receptor in dendritic cells prevents thymic atrophy in response to dioxin.

ABSTRACT: In nearly every species examined, administration of the persistent environmental pollutant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin, TCDD) causes profound immune suppression and thymic atrophy in an aryl hydrocarbon receptor (AhR) dependent manner. Moreover, TCDD alters the development and differentiation of thymocytes, resulting in decreases in the relative proportion and absolute number of double positive (DP, CD4⁺CD8⁺) thymocytes, as well as a relative enrichment in the relative proportion and absolute number of double negative (DN, CD4^-CD8^-) and single-positive (SP) CD4⁺CD8^- and CD4^-CD8⁺ thymocytes. Previous studies suggested that the target for TCDD-induced thymic atrophy resides within the hem

SUBMITTER: Beamer CA 

PROVIDER: S-EPMC6367717 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature