Regular Article2,3,7,8-Tetrachlorodibenzo-p-dioxin Does Not Directly Alter the Phenotype of Maturing B Cells in a Murine Coculture System
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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of immunity in THP-1-derived macrophages and the possible mechanisms
2021, Environmental PollutionCitation Excerpt :It is worth noting that there is no obvious dose-effect relationship in the production of part cytokines (Fig. 3). However, this is not rare that cytokines secretion does not always follow the increasing concentration or time of stimulation (Wyman et al., 2002; Podechard et al., 2008; Jensen et al., 2003; Ishimaru et al., 2009). Although the cytokines/chemokines have long been one of the most concerned research hot spots, it remains not entirely clear how these cytokines produced and interact.
The Aryl Hydrocarbon Receptor and Immunity
2018, Comprehensive Toxicology: Third EditionA single mid-gestation exposure to TCDD yields a postnatal autoimmune signature, differing by sex, in early geriatric C57BL/6 mice
2011, ToxicologyCitation Excerpt :The present mice showed multiple TCDD-related differences in B cells at 48 weeks-of-age including an increase in the earliest bone marrow B progenitor (B220loCD24−AA4.1+) and a decrease in total bone marrow-derived lymphoid cells expressing B220. The increase in the earliest B progenitor cells may agree with an increase in pre-pro-B cells detected in a S17 stromal line exposed to TCDD (Wyman et al., 2002). Functional or other changes in bone marrow B-lineage cells that may accompany these alterations in phenotypic distribution have not been studied but may be important.
The aryl hydrocarbon receptor has a normal function in the regulation of hematopoietic and other stem/progenitor cell populations
2009, Biochemical PharmacologyCitation Excerpt :That the effect was not specific for just the T-lymphoid precursor population was suggested by studies showing that numbers of cells in the immature B cell compartment also decreased following TCDD exposure [20]. However, the further differentiation of committed, but immature, B cells to more mature cells was not affected by the direct exposure of these cells to TCDD under culture conditions [21]. These studies suggested that either more immature progenitors or stem cells were directly affected by TCDD or that TCDD was targeting cell populations in the microenvironment in vivo that are, in part, responsible for directing B cell differentiation and which may not be active or present under culture conditions.
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To whom correspondence should be addressed at Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, 575 Elmwood Ave., Box EHSC, Rochester, NY 14642.