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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.

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1
Laboratoire de Physiologie Animale, Institut de Biologie et Médecine Moléculaire, Université Libre de Bruxelles, Belgium.

Abstract

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.

PMID:
18384884
DOI:
10.1016/j.imlet.2008.02.006
[Indexed for MEDLINE]

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