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Alpha-galactosylceramide modulates the induction of indoleamine 2,3-dioxygenase in antigen presenting cells.

Abstract：

:The glycolipid alpha-galactosylceramide (alpha-GalCer), when presented on CD1 molecules by antigen presenting cells (APCs) to invariant NKT (iNKT cells), is a potent immunomodulator. Indoleamine 2,3-dioxygenase (IDO), an enzyme catalyzing the catabolism of L-tryptophan along the kynurenine pathway, is inducible in APC and represents one of the main endogenous mechanisms of T cell homeostasis, peripheral tolerance and immunosuppression. No data have been published yet on the effect of alpha-GalCer on IDO in APC. We aimed to determine if: (1) alpha-GalCer modulates IDO in APC; (2) the alpha-GalCer-induced effect on IDO correlates with the production by APC of active compounds; (3) the medium from alpha-GalCer-treated APC is able to stimulate iNKT cells. From our results alpha-GalCer alone did not modify IDO expression (RT-PCR) in APC, but when human peripheral blood mononuclear cells (PBMC), monocytes, and monocytic cell lines (THP-1), expressing high levels of CD1d, were treated with interferon-gamma (IFN-gamma) plus alpha-GalCer a significant potentiation of IDO transcription was measured. This effect was not induced by increased IFN-gamma release by APC, and it was functionally correlated with increased L-kynurenine (L-KYN) release by alpha-GalCer-treated CD1d-transfected THP-1 cells. The medium of these cells stimulated iNKT hybridoma cells to release interleukin (IL)-2, while alpha-GalCer alone resulted ineffective. The data demonstrate that alpha-GalCer: (1) does not induce IFN-gamma release by APC; (2) potentiates IFN-gamma-induced IDO expression and function in APC; (2) requires CD1d molecules for inducing these effects; (3) induces the release by APC of compounds active in stimulating iNKT cells.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Fallarini S,Paoletti T,Panza L,Lombardi G

doi

10.1016/j.bcp.2008.07.001

subject

Has Abstract

pub_date

2008-09-15 00:00:00

pages

738-50

issue

6

eissn

0006-2952

issn

1873-2968

pii

S0006-2952(08)00461-9

journal_volume

76

pub_type

杂志文章

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