As recently reported by labroots, a team working at the University of Bonn found that a variety of substances in the intestines can bind to AHR, which in turn down-regulates the action of the immune response. An appropriate level of response by the immune system is critical and is under the control of AHR and its repressor.
Expanding on those findings, this new study, published in Nature Communications, has shown that AHR plays a role in the regulating how the immune system responds to viral infections.
The team at Hokkaido analyzed mouse cells that were deficient in AHR and compared them to normal cells containing AHR. They determined when the receptor is activated by amino acid metabolites, there is a reduction in the production of an antiviral protein called type I interferon (IFN-I).
The researchers found the receptor accomplishes that by activating the gene that encodes for a protein called TIPARP, TCDD inducible poly(ADP-ribose) polymerase. TIPARP subsequently interferes with the pathway (called the TBK1-mediated pathway) that normally stimulates interferon production after infection with a virus.
It is also proposed that identifying the factors and molecules that regulate the pathways stimulated by AHR activation could have clinical implications for controlling and treating pathological, dangerous innate immune responses.
Sources: Nature Immunology, AAAS/Eurekalert! via Hokkaido University