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We found that AHR is sensitive to cAMP signaling mediated by cAMP-dependent protein kinase (PKA) which fundamentally differs from AHR signaling mediated by the exogenous ligand dioxin.
Li et al. [5] observed that AhR signaling maintains numbers and functions of intraepithelial lymphocytes and innate lymphoid cells, and that AhR-deficiency increased epithelial vulnerability and immune activation in mice.
Also other studies have shown that AhR is required for the production of IL-22, supporting the importance of this relationship [17].
This study provides the first evidence that AhR expression is essential for the physiological regulation of cellular miRNA levels- including miR-196a.
The fact that AHR waned prior to resolution of AO indicates that AHR requires a sustained exposure to toxin, which would be typical of the infectious process.
It has been reported that AhR activity differs among cell types [24], [25], [26].
Together these observations suggest that AhR activation may be a cancer counteracting mechanism in the prostate.
Moreover, we noted that AhR expression is higher upon combining androgen ablation and β-TrCP inhibition.
Our observations that AHR and airway eosinophilia were both of transient nature irrespective of challenge protocol support this notion.
Indeed, it has been recently reported that AHR is expressed by lamprey lymphocytes that resemble T cells [35].
Unexpectedly, our data indicated that AhR does not require an exogenous ligand to stimulate αB-crystallin promoter activity.
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