English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Aryl hydrocarbon receptor (AHR) activation by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) is well established at suppressing humoral immunity. Previous studies in mouse B cells revealed that decreased IgM production was due to a significant suppression in the mRNA levels of the immunoglobulin M components (IgH, IgJ, and Igκ chains) and subsequent decrease in IgM synthesis. In contrast, the current study shows that activation of AHR in human B cells also results in a significant suppression of the number of IgM-secreting cells, but this is not due to a decrease in the transcription or translation of IgH, IgJ, and Igκ chains. Instead, the reduced humoral response is due to the impairment of IgM secretion. This is further evidenced by an accumulation of intracellular IgM in human B cells, which indicates that activation of AHR alters distinct regulatory pathways in human and mouse B cells leading to the suppressed primary IgM response. Collectively, these results demonstrate that although AHR activation mediates suppression of humoral immune responses across many different animal species, the mechanism of action is not necessarily conserved across species.

toxicological sciences

Suppression of the IgM Response by Aryl Hydrocarbon Receptor Activation in Human Primary B Cells Involves Impairment of Immunoglobulin Secretory Processes