NDLI: All-trans retinoic acid induces arginase-1 and inducible nitric oxide synthase-producing dendritic cells with T cell inhibitory function.

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All-trans retinoic acid induces arginase-1 and inducible nitric oxide synthase-producing dendritic cells with T cell inhibitory function.

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All-trans retinoic acid induces arginase-1 and inducible nitric oxide synthase-producing dendritic cells with T cell inhibitory function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hamilton, Thomas A. Qin, Jie Lu, Lina Qian, Shiguang Bhatt, Sumantha Fung, John J. Bennett, Carole
Description	Author Affiliation: Bhatt S ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195); Qin J ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195); Bennett C ( Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195); Qian S ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195); Fung JJ ( Department of General Surgery, Transplantation Center, Digestive Disease Institute, Cleveland Clinic, Cleveland, OH 44195.); Hamilton TA ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195); Lu L ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195)
Abstract	Hepatic stellate cells (HSC) are a major source of the immunoregulatory metabolite all-trans retinoic acid (ATRA), which may contribute to the generation of tolerogenic dendritic cells (DCs) in the liver. The present study seeks to clarify the mechanism(s) through which ATRA promotes the development of tolerogenic DCs. Although bone marrow-derived ATRA-treated DCs (RA-DCs) and conventional DCs had comparable surface phenotype, RA-DCs had diminished stimulatory capacity and could directly inhibit the expansion of DC/OVA-stimulated OT-II T cells. Arginase-1 (Arg-1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity, 2) the Arg-1 inhibitor N(w)-hydroxy nor-l-arginine partially reversed suppression, and 3) the suppressive function of RA-DCs was partially compromised using OT-II T cells from GCN2(-/-) mice, which are insensitive to Arg-1. Inducible NO synthase (iNOS), however, was found to be a more significant contributor to RA-DC function because 1) ATRA potentiated the expression of IFN-Î³-induced iNOS, 2) suppressive function in RA-DCs was blocked by the iNOS inhibitor N(G)-monomethyl-l-arginine, monoacetate salt, and 3) RA-DCs derived from iNOS(-/-) mice exhibited near complete loss of tolerogenic function, despite sustained Arg-1 activity. The expression of iNOS and the suppressive function of RA-DCs were dependent on both IFN-Î³ and ATRA. Furthermore, the in vivo behavior of RA-DCs proved to be consistent with their in vitro behavior. Thus, we conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-Î³-treated DCs, resulting in a tolerogenic phenotype. These findings elucidate mechanisms through which ATRA may contribute to liver immune tolerance.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303073
Journal	The Journal of Immunology
Issue Number	11
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antineoplastic Agents Pharmacology Arginase Immunology Bone Marrow Cells Dendritic Cells Immune Tolerance Drug Effects Nitric Oxide Synthase Type Ii Tretinoin Animals Genetics Gene Expression Regulation, Enzymologic Interferon-gamma Mice Mice, Knockout T-lymphocytes Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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All-trans retinoic acid induces arginase-1 and inducible nitric oxide synthase-producing dendritic cells with T cell inhibitory function.