Send to

Choose Destination
Immunol Lett. 2008 Jun 15;118(1):21-9. doi: 10.1016/j.imlet.2008.02.006. Epub 2008 Mar 14.

Normal development and function of dendritic cells in mice lacking IDO-1 expression.

Author information

Laboratoire de Physiologie Animale, Institut de Biologie et Médecine Moléculaire, Université Libre de Bruxelles, Belgium.


Dendritic cells (DCs) have been shown to express the tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO-1), a protein presently thought to exert dual and possibly contrasting effects on the immune response. Depletion of tryptophan and release of tryptophan catabolites have been shown to exert a tolerogenic influence on T cell responses, while the IDO enzymatic activity has been recently suggested to promote DC maturation. In this report, we have explored the putative role of IDO-1 in regulating DC biology by analyzing DC development and function from IDO-1 deficient mice. In keeping with previous observations, lack of IDO-1 expression was found to affect in vitro DC generation from bone mouse precursors cultured in the presence of GM-CSF. However, change in growth factor (Flt3L) and/or culture conditions (low-adherence vessels) abolished the difference observed between wt (wild type) and IDO-1-deficient, in vitro generated DCs. Moreover, IDO-1-deficient mice displayed a normal DC compartment in vivo, suggesting that IDO-1 does not play a significant role in DC development and function in vivo. Collectively, these observations suggest that despite a possible role for IDO-1 expression in regulating DC differentiation in vitro under commonly used culture conditions, IDO-1 is largely dispensable for DC development and function in vivo.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center