| First Author | Nakajima R | Year | 2018 |
| Journal | J Invest Dermatol | Volume | 138 |
| Issue | 10 | Pages | 2195-2204 |
| PubMed ID | 29605671 | Mgi Jnum | J:266435 |
| Mgi Id | MGI:6202844 | Doi | 10.1016/j.jid.2018.03.1520 |
| Citation | Nakajima R, et al. (2018) Exacerbated Immune Complex-Mediated Vascular Injury in Mice with Heterozygous Deficiency of Aryl Hydrocarbon Receptor through Upregulation of Fcgamma Receptor III Expression on Macrophages. J Invest Dermatol 138(10):2195-2204 |
| abstractText | Aryl hydrocarbon receptor (AhR), which was discovered as a receptor for environmental concomitants, plays an important role widely in the immune system. In this study, we assessed AhR involvement in immune-complex-mediated vascular injury by examining the reverse-passive Arthus reaction in AhR heterozygous knockout (AhR(+/-)) mice. In the cutaneous Arthus reaction, dermal edema was severer in AhR(+/-) mice than in wild-type mice. The number of infiltrating neutrophils and mRNA expression levels of CXC chemokine ligand 1 and IL-6 were also increased in AhR(+/-) mice. Similarly, in the peritoneal Arthus reaction, infiltration of neutrophils was increased in AhR(+/-) mice. Peritoneal macrophages from AhR(+/-) mice expressed higher levels of Fcgamma receptor III and produced higher levels of CXC chemokine ligand 1 and IL-6 after immune complex treatment. In addition, AhR occupied the promoter regions of Fcgamma receptor III gene in peritoneal macrophages in a ligand-dependent manner. Depletion of macrophages reduced the cutaneous Arthus reaction in AhR(+/-) mice, and adoptive transfer of AhR(+/-) mice macrophages into wild-type mice exacerbated the peritoneal Arthus reaction. Furthermore, AhR expression was decreased and Fcgamma receptor III expression was increased in CD14(+) monocytes in peripheral blood from patients with immune-complex-mediated vasculitis compared with those from healthy controls. These results suggest that downregulation of AhR is associated with the exacerbation of immune-complex-mediated vascular injury. |
