T lymphocytes are direct, aryl hydrocarbon receptor (AhR)-dependent targets of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): AhR expression in both CD4+ and CD8+ T cells is necessary for full suppression of a cytotoxic T lymphocyte response by TCDD.

The cellular basis for the potent suppression of T cell-mediated immune responses in mice following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is not fully understood. Although activation of the aryl hydrocarbon receptor (AhR) is required, the specific AhR+ cells that transduce the suppression have been difficult to identify in vivo. The recent availability of AhR-/- mutant mice has provided a resource for novel approaches to investigate the direct targets of TCDD.

Inhibition of TC-1 cytokine production, effector cytotoxic T lymphocyte development and alloantibody production by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental contaminant and prototypic ligand for the aryl hydrocarbon receptor, is a potent immunotoxicant. To understand the underlying mechanisms of TCDD immunotoxicity, we have characterized the time course of changes in CTL, alloantibody, and cytokine responses to the P815 tumor allograft in C57B1/6 mice treated with 0 or 15 microg TCDD/kg. Suppression of CTL activity by TCDD directly correlated with reduced numbers of splenic CTL effector cells identified by their CD8+CD44 high CD45RB low phenotype, while suppression of the alloantibody response correlated with a lack of expansion of the B220+ splenocyte population.

Polychlorinated biphenyl-induced suppression of cytotoxic T lymphocyte activity: role of prostaglandin-E2.

Prostaglandin-E2 (PGE2) was investigated for its role in suppression of splenic cytotoxic T lymphocyte (CTL) activity following exposure to 3,3',4,4',5,5'-hexachlorobiphenyl (HxCB) in mice. Following i.p.

Acute inflammatory response to sheep red blood cells in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin: the role of proinflammatory cytokines, IL-1 and TNF.

Recent studies have demonstrated that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure of C57Bl/6 mice results in an enhanced inflammatory response to intraperitoneal injection of sheep red blood cells (SRBC). This response is characterized by an increase in total peritoneal cells (PEC) as well as an increase in relative and absolute numbers of neutrophils (PMN) harvested 16 to 40 hr following injection of SRBC. The mechanisms whereby TCDD increases cellular influx are unknown.

Immunologic and endocrine effects of the flame-retardant pentabromodiphenyl ether (DE-71) in C57BL/6J mice.

Polybrominated diphenyl ethers are manufactured for use as flame retardants in commercial plastics and textiles in Europe and North America. These studies investigated the acute and subchronic immunotoxicity and endocrine effects of a commercial pentabromodiphenyl either mixture, DE-71, in female C57BL/6 mice. Mice were orally exposed to acute single doses of DE-71 of 0, 0.