Direct suppression of antibody responses by chlorinated dibenzodioxins in cultured spleen cells from (C57BL/6 × C3H)F1 and DBA/2 mice
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Cited by (81)
The Aryl Hydrocarbon Receptor and Immunity
2018, Comprehensive Toxicology: Third EditionSHP-1 is directly activated by the aryl hydrocarbon receptor and regulates BCL-6 in the presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
2016, Toxicology and Applied PharmacologyCitation Excerpt :The effect diminished when TCDD was added at days 2–5 post-antigen sensitization (Tucker et al., 1986). In addition, the suppression of the LPS-induced IgM antibody forming cell (AFC) response was produced when TCDD was added before 3 h post-B cell activation (Holsapple et al., 1986). Suppression of early kinase phosphorylation by TCDD, especially kinases associated with the CD40 receptor and cytokine signaling pathways may provide an explanation for the window of sensitivity surrounding the effects observed in human cells.
All-or-none suppression of B cell terminal differentiation by environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin
2013, Toxicology and Applied PharmacologyCitation Excerpt :The fraction of IgMhigh cells was maximally suppressed at 30 nM TCDD, reaching only about one third of the vehicle control. It is important to emphasize that consistent with earlier reports (Crawford et al., 2003; Holsapple et al., 1986), TCDD had no effect on LPS-induced proliferation (Fig. S3A). Cell viability was also unaffected (result not shown).
Regulation of Bach2 by the aryl hydrocarbon receptor as a mechanism for suppression of B-cell differentiation by 2,3,7,8-tetrachlorodibenzo-p-dioxin
2011, Toxicology and Applied PharmacologyCitation Excerpt :Although TCDD affects multiple aspects of the immune system, cell-type fractionation reconstitution studies of heterogeneous leukocyte preparations have shown that B cells are the primary cellular targets involved in suppression of the humoral immune response (Dooley and Holsapple, 1988). Other studies have shown that direct addition of TCDD to naïve primary B cells or B-cell lines suppresses immunoglobulin M (IgM) secretion, suggesting that TCDD impairs the differentiation of B cells to IgM secreting plasma cells (Holsapple et al., 1986; Morris et al., 1993; Sulentic et al., 1998). Most of the biological effects of TCDD including the suppression of the humoral immune response are mediated through the activation of the aryl hydrocarbon receptor (AHR) (Sulentic et al., 1998; Gu et al., 2000).
Complete blood cell counts and blood chemistry in Yusho
2005, Journal of Dermatological Science, Supplement