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© 1990 Oxford University Press

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Role of the Ah Locus in Suppression of Cytotoxic T Lymphocyte Activity by Halogenated Aromatic Hydrocarbons (PCBs and TCDD): Structure-Activity Relationships and Effects in C57BI/6 Mice Congenic at the Ah Locus

N. I. KERKVLIET*,{dagger},1, B. B. SMITH*, L. BAECHER STEPPAN*, J. A. YOUNGBERG*, M. C. HENDERSON{dagger} and D. R. BUHLER{dagger}

*College of Veterinary Medicine Corvallis, Oregon 97331 {dagger}Environmental Health Sciences Center, Oregon State University Corvallis, Oregon 97331

Received May 30, 1989; accepted November 8, 1989

Role of the Ah Locus in Suppression of Cytotoxic T Lymphocyte Activity by Halogenated Aromatic Hydrocarbons (PCBs and TCDD): Structure-Activity Relationships and Effects in C57B1/6 Mice Congenic at the Ah Locus. KERKVLIET, N. I., BAECHER-STEPPAN, L., SMITH, B. B., YOUNGBERG, J. A., HENDERSON, M. C, AND BUHLER, D. R. (1990). Fundam. Appl. Toxicol. 14, 532–541. Previous studies have shown that the generation of cytotoxic T lymphocytes (CTL) following allogeneic tumor challenge is suppressed in Ah-responsive C57B1/6 mice treated with a single oral dose of the toxic, Ah receptor-binding 3,4,5,3',4',5'-hexachlorobiphenyl (HxCB). The present studies have examined the specific role of the Ah receptor in this immuno-toxic response by utilizing HxCB isomers of known, varied affinity for the Ah receptor as well as by comparing effects of high-affinity Ah receptor ligands (3,4,5,3',4',5'-HxCB and 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD]) on the CTL response of mice that differ only at the Ah locus, that is, Ah-responsive (Ah1*) and Ah-nonresponsive (Ahdd) congenic C57B1/6 mice. Correlative changes in thymic weight, serum corticosterone (CS) levels, and spleen cellularity were also measured. The potency of HxCB congeners (3,4,5,3',4',5'-; 2,3,4,5,3',4'-; 2,4,5,2',4',5'-) and 2,3,7,8-TCDD to suppress the CTL response, to reduce spleen cellularity, to cause thymic atrophy, and to elevate serum CS levels was directly correlated with the binding affinity of the congener for the Ah receptor. Furthermore, these parameters of immunotoxicity in Ah*1 C57B1/6 mice were significantly more resistant to alterations induced by either 3,4,5,3',4',5'-HxCB or 2,3,7,8-TCDD as compared to Ah1* C57B1/6 mice. These results strongly support an Ah receptor-dependent immunotoxic mechanism in suppression of the CTL response following acute exposure to halogenated aromatic hydrocarbons.


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