Review articleA review of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced changes in immunocompetence: 1991 update
References (108)
- et al.
Immune alterations
- et al.
Mechanism of action and structure-activity relationship for the chlorinated dibenzo-p-dioxins and related compounds
- et al.
Polychlorinated biphenyl immunotoxicity: defence on isomer planarity and the Ah gene complex
Toxicol. Appl. Pharmacol.
(1982) - et al.
Development of a testing battery to assess chemical-induced immunotoxicity: national toxicology program's guidelines for immunotoxicity evaluation in mice
Fundam. Appl. Toxicol.
(1988) - et al.
Evidence for direct action of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thymic epithelium
Toxicol. Appl. Pharmacol.
(1985) - et al.
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD): Results of a 13-week oral toxicity study in rats
Toxicol. Appl. Pharmacol.
(1976) - et al.
Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) IN C57BL/6 mice
Toxicol. Appl. Pharmacol.
(1974) - et al.
Immunologic response and factors affecting its assessment
Environ. Health Perspect.
(1976) - et al.
Chemical separation of helper cell function and delayed hypersensitivity responses
Cell Immunol.
(1978) - et al.
Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment in vivo on thymocyte functions in mice after activation in vitro
Int. J. Immunopharmacol.
(1990)
The comparative toxicity of chlorinated dibenzo-p-dioxins in mice and guinea pigs
Toxicol. Appl. Pharmacol.
Role of the endocrine system in the action of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the thymus
Toxicology
Studies on 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced suppression and decreased resistance to infection: endotoxin hypersensitivity, serum zinc concentrations and effect of thymosin treatment
Toxicology
Flow cytometric analysis of lymphocyte subpopulations in the spleen and thymus of mice exposed to an acute immunosuppressive dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
Environ. Res.
Cellular and genetic basis for suppression of cytotoxic T cell generation by haloaromatic hydrocarbons
Immunopharmacology
Elucidation of cellular targets responsible for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of antibody responses: I. The role of the B lymphocyte
Immunopharmacology
Elucidation of cellular targets responsible for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of antibody responses: II. The role of the T lymphocyte
Immunopharmacology
Correlation of murine susceptibility to tumor, parasite and bacterial challenge with altered cell-mediated immunity following systemic exposure to the tumor promoter phorbol myristate acetate
Int. J. Immunopharmacol.
Sensitivity to suppression of cytotoxic T cell generation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is dependent on the Ah genotype of the murine host
Toxicol. Appl. Pharmacol.
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 C57BL/6 mice congenic at the Ah locus
Fundam. Appl. Toxicol.
Immunosuppressive effects of 2,3,7,8-tetrachlorobidenzo-p-dioxin in strains of mice with different susceptibility to induction of aryl hydrocarbon hydroxylase
Toxicol. Appl. Pharmacol.
Effect of Inducers of P-450 cytochrome isozymes on TCDD immunosuppressive activity
Chemosphere
Immunosuppression without liver induction by subchronic exposure to 2,7-dichlordibenzo-p-dioxin in adult female B6C3F1 mice
Toxicol. Appl. Pharmacol.
Direct suppression of antibody responses by chlorinated dibenzodioxins in cultured spleen cells from 9C57BL/6 × C3H)F1 and DBA/2 mice
Immunopharmacology
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced immunotoxicity
Int. J. Immunopharmacol.
Mechanisms of 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD)-induced humoral immune supression: evidence of primary defect in T-cell regulation
Toxicol. Appl. Pharmacol.
Influence of the Ah locus on the humoral immunotoxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin: Evidence for Ah-receptor-dependent and Ah-receptor-independent mechanisms of immunosuppression
Toxicol. Appl. Phamacol.
Production of human B and T cell growth factors is enhanced by thymic hormoones
Immunopharmacology
Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on IgA serum and bile levels in rats
Immunopharmacology
Examination of bone marrow, immunologic parameters and host susceptibility following pre- and postnatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
Int. J. Immunopharmacol.
Acute myelotoxic responses in mice exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
Toxicol. Appl. Pharmacol.
Selective inhibition of polymorphonyuclear neutrophil activity by 2,3,7,8-tetrachlorodibenzo-p-dioxin
Toxicol. Appl. Pharmacol.
Characteristics of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced endotoxin hypersensitivity: association with hepatotoxicity
Toxicology
Modulation of serum complement levels following exposure to polychlorinated dibenzo-p-dioxins
Toxicol. Appl. Pharmacol.
Differential toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57BL/6L mice congenic at the Ah locus
Fundam. Appl. Toxicol.
Immune abnormalities associated chronic exposure in Rhesus
Chemosphere
Immunotoxicity studies of PCB (Aroclor 1254) in the adult rhesus (Macaca Mulatta monkey—preliminary report
Int. J. Immunopharmacol.
Immunologic evaluation of patients with polychlorinated biphenyl poisoning: determination of lymphocyte subpopulations
Toxicol. Appl. Pharmacol.
Immune alterations
Immunological effects following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin: a review
Dioxin-induced thymic atrophy and suppression of thymus-dependent immunity
In vivo and in vitro effects of TCDD on stem cell and B cell differentiation
Dose response, time-course and mechanism for suppression of cytotoxic T cell generation by 2,3,7,8-tetrachlorodibenzo-p-dioxin
A proposed model for the actions of TCDD on epidermal and thymic epithelial target cells
2,3,7,8-tetrachlorodibenzo-p-dioxin and related halogenated aromatic hydrocarbons: examination of the mechanism of toxicity
Annu. Rev. Pharmacol. Toxicol.
Comparative toxicology and mechanism of action of polychlorinated dibenzo-p-dioxins and dibenzofurans
Annu. Rev. Toxicol.
The Ah locus: genetic differences in toxicity, cancer, mutation and birth defects
Crit. Rev. Toxicol.
The regulation of gene expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin
Pharmacol. Rev.
Genetic and molecular aspects of2,3,7,8-tetrachlorodibenzo-p-dioxin action
Annu. Rev. Pharmacol. Toxicol.
2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced changes in immunocompetence: Possible mechanisms
Annu. Rev. Pharmacol. Toxicol.
Cited by (195)
Pesticide use and risk of systemic autoimmune diseases in the Agricultural Health Study
2022, Environmental ResearchRecent advances in the bio-remediation of persistent organic pollutants and its effect on environment
2018, Journal of Cleaner ProductionAHR and the issue of immunotoxicity
2018, Current Opinion in ToxicologyCitation Excerpt :Finally, we consider the parameters, which must be integrated to predict beneficial versus adverse effects of ligands and AHR signaling on the immune system. With regard to the immune system, it has long been known that activating the AHR with certain xenobiotic chemicals, such as PAHs or HAHs, can result in immunotoxicity [9,10]. PAHs and HAHs usually occur in mixtures in the environment (air, soil, water), where they are generated by incomplete combustion processes, such as forest fires, burning of wood or fossil fuels, waste incineration, car exhausts, smoking, or the grilling of meat.
Biochemical and physiological effects from exhaust emissions. A review of the relevant literature
2016, PathophysiologyCitation Excerpt :IgE and IgG4 represent the primary interface of triggered antibodies [93,102,103], which in turn trigger a cascade of cytokine expression at the inflammation site. This reaction path, which is overexpressed in allergic and asthmatic individuals, is followed by B-cell and T-cell triggering, both of which can in turn be suppressed by particular PAH types [104–106]. The expression of the above-mentioned antibodies is responsible for the triggering of interleukins, particularly IL-4, IL-5, IL-6, IL-8, and IL-10 [93,103].