Ah receptor mediated suppression of the antibody response in mice is primarily dependent on the Ah phenotype of lymphoid tissue

Silkworth, Jay B.; Antrim, LuAnn; Sack, G.

doi:10.1016/0041-008x(86)90365-0

Cited by 48 publications

(7 citation statements)

References 25 publications

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“…However, it should not be construed that the Ah locus is the only factor that controls HAH-induced suppression of the antibody response to SRBC. Thus, the AFC response of Ah-responsive chimeric BALB/c mice that received bone marrow from Ah-nonresponsive DBA/2 mice was reduced in a dose-dependent manner following exposure to 3,4,3',4' tetrachlorbiphenyl although the degree of suppression was not statistically significant (150). It is also apparent that nonAh-receptor ligands such as 2,7-dichlordibenzo-p-dioxin may be immunosuppressive by mechanisms unrelated to the Ah locus (64).…”

Section: Exon Kerkvliet and Talcottmentioning

confidence: 76%

“…Likewise, the ability of different PCB or PCDD congeners to suppress the antiSRBC response is correlated with their ability to bind the Ah receptor (79,151). More recently, Silkworth et al (150) have used radiation chimeras to show that the Ah phenotype of the lymphoid cells is the primary determinant of sensitivity to PCB-induced humoral immune suppression rather than the Ah phenotype of the host in general. However, it should not be construed that the Ah locus is the only factor that controls HAH-induced suppression of the antibody response to SRBC.…”

Section: Exon Kerkvliet and Talcottmentioning

confidence: 96%

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Immunotoxicity of carcinogenic pesticides and related chemicals

Exon

Kerkvliet

Talcott

1987

Environmental Carcinogenesis Reviews

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Section: Exon Kerkvliet and Talcottmentioning

confidence: 76%

Section: Exon Kerkvliet and Talcottmentioning

confidence: 96%

Immunotoxicity of carcinogenic pesticides and related chemicals

Exon

Kerkvliet

Talcott

1987

Environmental Carcinogenesis Reviews

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“…Similarly, the halogenated hydrocarbons, 3,3′,4,4′-tetrachlorobiphenyl and 2,3,3′,4,4′,5-hexachlorobiphenyl, suppressed antibody responses to challenge with lipopolysaccharide (LPS) or sheep red blood cells [ 27 , 28 ]. At least some of this apparent suppression of B cell differentiation induced by PAHs and PCBs was dependent on the degree to which the AhR ligand could be metabolized [ 22 , 23 , 29 ].…”

Section: Environmental Chemicals As Probes For Ahr Control Of B Cell mentioning

confidence: 99%

The role of the aryl hydrocarbon receptor in normal and malignant B cell development

Sherr

Monti

2013

Semin Immunopathol

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The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor historically studied for its role in environmental chemical-mediated toxicity and carcinogenicity. In the last 5 years, however, it has become clear that the AhR, presumably activated by endogenous ligand(s), plays an important role in immune system development and function. Other articles in this edition summarize AhR function during T cell and antigen-presenting cell development and function, including the effects of AhR activation on dendritic cell function, T cell skewing, inflammation, and autoimmune disease. Here, we focus on AhR expression and function during B cell differentiation. Studies exploiting immunosuppressive environmental chemicals to probe the role of the AhR in humoral immunity are also reviewed to illustrate the multiple levels at which a “nominally activated” AhR could control B cell differentiation from the hematopoietic stem cell through the pro-B cell, mature B cell, and antibody-secreting plasma cell stages. Finally, a putative role for the AhR in the basic biology of B cell malignancies, many of which have been associated with exposure to environmental AhR ligands, is discussed.

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“…It i s well known that lymphoid atrophy following exposure to planar HAHs correlates with binding affinity to the Ah-R (Poland & Glover, 1980;Nebert & Eiscn, 1984;Silkworth et al, 1986). The intracellular binding of a planar PCB to Ah-R i s followed by a cascade of events including the transcription and subsequent synthesis of a variety of gene products.…”

Section: Thymus and Liver Weightsmentioning

confidence: 99%

Tributyltin Potentiates 3,3',4,4',5-Pentachlorobiphenyl-Induced Cytochrome P-4501a-Related Activity

Delong¹,

Rice²

1997

Journal of Toxicology and Environmental Health

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~i s s i s s i~~y~t a t e , Mississippi, USA Induction of cytochrome P-4501A protein and induction of related enzyme activity are hallmark physiological responses following exposure to planar halogenated aromatic hydrocarbons (HAHs) such as 3,3',4,4', PeCB). Environments contaminated by HAHs are often contaminated by mixtures of anthropogenic contami-I nants, including organometallic compounds. Both HAHs and ~r~anometallics easily bioconcentrate and bioaccumulate in aquatic food chains that may ultimately be linked to humans through seafood consumpti&. Tributyltin (TBT), a marine biocjde, has been detected in many aquatic environments due to its primary use as a marine antifoulant agent. Exposure to TBT, as well as several PCBs, has been associated with immunotoxicity, neurotoxicity, and endocrine disruption. Recently TBT has been shown to inhibit cyte chrome P-4501A activity in vitro, but information concerning these effects in vivo and in combination with classical inducers of P-4501A, such PeCB, is lacking. We exposed female B6C3Fl mice to 0.01, 0.1, and 1.0 mg/kg PeCB, TBT, or both in combination, with corn oil (CO) serving as a carrier control. Cytochrome P-4501A protein levels and related benzo[alpyrene hydroxylation (BaP-OHase) activity were measured following a single acute intraperitoneal (ip) dose or seven daily injections. Body, thymus, and liver weights were used to monitor general physiological responses following exposure. P-4501A levels and BaP-OHase activity were significantly elevated in mice exposed to PeCB alone. This effect was enhanced by coexposure to low levels of TBT; PeCB-induced P-450lA-related activity was potentiated at the low range of each. The highest dose of TBT, however, inhibited these activities when given in combination with PeCB. Thymic atrophy was evident only in mice exposed daily to 0.1 and 1.0 mg/kg PeCB alone, or to a combination of the lowest and highest dose of PeCB and TBT, respectively. Because environmental levels of TBT are not expected to be as high as the highest level used in our toxicological studies, we conclude that environmental exposure to TBT may potentiate, rather than inhibit, the activity of environmental levels of HAHs that are associated with P-450 1A induction.

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Ah receptor mediated suppression of the antibody response in mice is primarily dependent on the Ah phenotype of lymphoid tissue

Cited by 48 publications

References 25 publications

Immunotoxicity of carcinogenic pesticides and related chemicals

Immunotoxicity of carcinogenic pesticides and related chemicals

The role of the aryl hydrocarbon receptor in normal and malignant B cell development

Tributyltin Potentiates 3,3',4,4',5-Pentachlorobiphenyl-Induced Cytochrome P-4501a-Related Activity

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