Kehong Hao and Qian Zhou contributed equally to this work.
Possible role of the ‘IDO-AhR axis’ in maternal-foetal tolerance†
Article first published online: 2 JAN 2013
© 2013 International Federation for Cell Biology
Cell Biology International
Volume 37, Issue 2, pages 105–108, February 2013
How to Cite
Hao, K., Zhou, Q., Chen, W., Jia, W., Zheng, J., Kang, J., Wang, K. and Duan, T. (2013), Possible role of the ‘IDO-AhR axis’ in maternal-foetal tolerance. Cell Biology International, 37: 105–108. doi: 10.1002/cbin.10023
- Issue published online: 21 JAN 2013
- Article first published online: 2 JAN 2013
- Accepted manuscript online: 17 DEC 2012 11:30AM EST
- Manuscript Accepted: 19 NOV 2012
- Manuscript Received: 9 OCT 2012
- maternal-foetal tolerance;
- Treg cells
The induction and maintenance of immunologic tolerance at the feto-maternal interface is necessary for a successful pregnancy. The most accepted hypothesis for the mechanism underlying this tolerance is that pregnancy-induced foetal antigen-specific maternal T regulatory (Treg) cells mediate maternal tolerance to the foetus. The aryl hydrocarbon receptor (AhR), which is highly expressed in the placenta, is widely studied in female reproductive biology and immunology. Activation of AhR can promote immune tolerance by controlling the differentiation of Treg cells in some autoimmune disorders. However, the specific mechanisms underlying tolerance are poorly understood. Indoleamine 2,3-dioxygenase (IDO) is the initial and rate-limiting enzyme of tryptophan catabolism in human placental trophoblasts. IDO produces kynurenine, an endogenous AhR ligand that directly activates AhR and is proposed to be central to the establishment and maintenance of immunologic tolerance at the maternal-foetal interface. We propose that kynurenine activates AhR, leading to the AhR-dependent Treg cells generation, which in turn critically regulates immunological tolerance at the feto-maternal interface. This hypothesis must be tested and the proof of this hypothesis may provide a potential therapeutic target for the treatment of infertility and other adverse pregnancy outcomes resulted from inadequate immunological tolerance at the feto-maternal interface.