NDLI: Nitric oxide-induced regulatory T cells inhibit Th17 but not Th1 cell differentiation and function.

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Nitric oxide-induced regulatory T cells inhibit Th17 but not Th1 cell differentiation and function.

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Nitric oxide-induced regulatory T cells inhibit Th17 but not Th1 cell differentiation and function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mitani, Akio Niedbala, Wanda Fukada, Sandra Y. Liew, Foo Y. Pushparaj, Peter Nascimento, Daniela Alqahtani, Mohammed H. Jiang, Hui R. Besnard, Anne-Gaelle Alves-Filho, Jose C.
Description	Country affiliation: United kingdom Author Affiliation: Niedbala W ( Centre of Immunology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom. wanda.niedbala@glasgow.ac.uk)
Abstract	NO is a free radical with pleiotropic functions. We have shown earlier that NO induces a population of CD4(+)CD25(+)Foxp3(-) regulatory T cells (NO-Tregs) that suppress the functions of CD4(+)CD25(-) effector T cells in vitro and in vivo. We report in this study an unexpected finding that NO-Tregs suppressed Th17 but not Th1 cell differentiation and function. In contrast, natural Tregs (nTregs), which suppressed Th1 cells, failed to suppress Th17 cells. Consistent with this observation, NO-Tregs inhibited the expression of retinoic acid-related orphan receptor Î³t but not T-bet, whereas nTregs suppressed T-bet but not retinoic acid-related orphan receptor Î³t expression. The NO-Treg-mediated suppression of Th17 was partially cell contact-dependent and was associated with IL-10. In vivo, adoptively transferred NO-Tregs potently attenuated experimental autoimmune encephalomyelitis. The disease suppression was accompanied by a reduction of Th17, but not Th1 cells in the draining lymph nodes, and a decrease in the production of IL-17, but an increase in IL-10 synthesis. Our results therefore demonstrate the differential suppressive function between NO-Tregs and nTregs and indicate specialization of the regulatory mechanism of the immune system.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202580
Journal	The Journal of Immunology
Issue Number	1
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Immunology Growth Inhibitors Physiology Nitric Oxide T-lymphocytes, Regulatory Th1 Cells Th17 Cells Animals Cell Communication Cells, Cultured Pharmacology Immune Tolerance Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Primary Cell Culture Cytology Comparative Study Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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