The aromatic hydrocarbon receptor (AhR)-dependent pathway involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced immunotoxicity has been studied extensively, but the AhR-independent molecular mechan-ism has not. In previous studies we found that the AhR is not expressed in L-MAT, a human lymphoblastic T-cell line. In this report, we provide the following evidence that the protein kinase C (PKC)hactivity is func-tionally involved in the AhR-independent signal transduction mechanism that participates in the TCDD-induced L-MAT cell apoptosis
