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Various transcription factors are also known to enhance or suppress T helper type 17 (Th17) differentiation. We have shown previously that the development of collagen-induced arthritis was suppressed in T-bet transgenic (T-bet Tg) mice, and T-bet seemed to suppress Th17 differentiation through an interferon (IFN)-γ-independent pathway, although the precise mechanism remains to be clarified. The present study was designed to investigate further the mechanisms involved in the regulation of Th17 differentiation by T-bet over-expression, and we found the new relationship between T-bet and aryl hydrocarbon receptor (AHR). Both T-bet Tg mice and IFN-γ -/- -over-expressing T-bet (T-bet Tg/IFN-γ -/- ) mice showed inhibition of retinoic acid-related orphan receptor (ROR)γt expression and IL-17 production by CD4 + T cells cultured under conditions that promote Th-17 differentiation, and decreased IL-6 receptor (IL-6R) expression and signal transducer and activator of transcription-3 (STAT-3) phosphorylation in CD4 + T cells. The mRNA expression of ahr and rorc were suppressed in CD4 + T cells cultured under Th-17 conditions from T-bet Tg mice and T-bet Tg/IFN-γ -/- mice. CD4 + T cells of wild-type (WT) and IFN-γ -/- mice transduced with T-bet-expressing retrovirus also showed inhibition of IL-17 production, whereas T-bet transduction had no effect on IL-6R expression and STAT-3 phosphorylation. Interestingly, the mRNA expression of ahr and rorc were suppressed in CD4 + T cells with T-bet transduction cultured under Th17 conditions. The enhancement of interleukin (IL)-17 production from CD4 + T cells by the addition of AHR ligand with Th17 conditions was cancelled by T-bet over-expression. Our findings suggest that T-bet over-expression-induced suppression of Th17 differentiation is mediated through IFN-γ-independent AHR suppression.

Titel:	T-bet over-expression regulates aryl hydrocarbon receptor-mediated T helper type 17 differentiation through an interferon (IFN)γ-independent pathway.
Autor/in / Beteiligte Person:	Yokosawa, M ; Kondo, Y ; Tahara, M ; Iizuka-Koga, M ; Segawa, S ; Kaneko, S ; Tsuboi, H ; Yoh, K ; Takahashi, S ; Matsumoto, I ; Sumida, T
Link:	Full Text Finder (Volltext)
Zeitschrift:	Clinical and experimental immunology, Jg. 188 (2017-04-01), Heft 1, S. 22-35
Veröffentlichung:	2022- : Oxford : Oxford University Press ; <i>Original Publication</i>: Oxford : Blackwell Scientific Publications, 2017
Medientyp:	academicJournal
ISSN:	1365-2249 (electronic)
DOI:	10.1111/cei.12912
Schlagwort:	Animals Arthritis, Experimental genetics Arthritis, Experimental immunology Arthritis, Experimental metabolism Arthritis, Experimental pathology Cells, Cultured Disease Models, Animal Immunomodulation Immunophenotyping Interferon-gamma genetics Interleukin-6 metabolism Mice Mice, Knockout Mice, Transgenic Models, Biological STAT3 Transcription Factor metabolism T-Lymphocyte Subsets cytology T-Lymphocyte Subsets immunology T-Lymphocyte Subsets metabolism Th17 Cells immunology Transduction, Genetic Cell Differentiation genetics Gene Expression Interferon-gamma metabolism Receptors, Aryl Hydrocarbon metabolism Signal Transduction T-Box Domain Proteins genetics Th17 Cells cytology Th17 Cells metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Clin Exp Immunol] 2017 Apr; Vol. 188 (1), pp. 22-35. <i>Date of Electronic Publication: </i>2017 Jan 31. MeSH Terms: Cell Differentiation* / genetics ; Gene Expression* ; Signal Transduction* ; Interferon-gamma / metabolism ; Receptors, Aryl Hydrocarbon / metabolism ; T-Box Domain Proteins / genetics ; Th17 Cells / cytology ; Th17 Cells / *metabolism ; Animals ; Arthritis, Experimental / genetics ; Arthritis, Experimental / immunology ; Arthritis, Experimental / metabolism ; Arthritis, Experimental / pathology ; Cells, Cultured ; Disease Models, Animal ; Immunomodulation ; Immunophenotyping ; Interferon-gamma / genetics ; Interleukin-6 / metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Models, Biological ; STAT3 Transcription Factor / metabolism ; T-Lymphocyte Subsets / cytology ; T-Lymphocyte Subsets / immunology ; T-Lymphocyte Subsets / metabolism ; Th17 Cells / immunology ; Transduction, Genetic References: Nat Immunol. 2008 Nov;9(11):1297-306. (PMID: 18849990) ; Science. 2002 Jan 11;295(5553):338-42. (PMID: 11786644) ; Nature. 2008 May 8;453(7192):236-40. (PMID: 18368049) ; Gastroenterology. 2011 Jul;141(1):237-48, 248.e1. (PMID: 21600206) ; J Invest Dermatol. 2008 Jul;128(7):1821-9. (PMID: 18185532) ; Nature. 2008 May 1;453(7191):65-71. (PMID: 18362915) ; Nat Immunol. 2008 Jun;9(6):641-9. (PMID: 18454151) ; Cell. 2006 Sep 22;126(6):1121-33. (PMID: 16990136) ; Proc Natl Acad Sci U S A. 2011 Aug 23;108(34):14222-7. (PMID: 21825138) ; Trends Immunol. 2002 Feb;23(2):96-101. (PMID: 11929133) ; J Immunol. 2013 Dec 15;191(12):5925-32. (PMID: 24249732) ; Nature. 2008 May 1;453(7191):106-9. (PMID: 18362914) ; Nature. 2010 Apr 29;464(7293):1381-5. (PMID: 20383124) ; Nat Immunol. 2007 Sep;8(9):958-66. (PMID: 17676043) ; Nat Immunol. 2014 Aug;15(8):758-66. (PMID: 24973819) ; Immunity. 2011 Dec 23;35(6):919-31. (PMID: 22195747) ; J Exp Med. 2011 May 9;208(5):1001-13. (PMID: 21518797) ; J Immunol. 2010 Feb 1;184(3):1552-9. (PMID: 20028652) ; Int Immunopharmacol. 2004 May;4(5):669-77. (PMID: 15120651) ; Nat Immunol. 2002 Jun;3(6):549-57. (PMID: 12006974) ; Cancer Res. 2008 May 15;68(10):3609-17. (PMID: 18483242) ; J Immunol. 2008 Mar 15;180(6):3746-56. (PMID: 18322180) ; J Exp Med. 2008 Jun 9;205(6):1369-79. (PMID: 18474630) ; Nat Rev Immunol. 2009 Feb;9(2):91-105. (PMID: 19151746) ; J Immunol. 1997 Jun 1;158(11):5501-6. (PMID: 9164973) ; Nat Immunol. 2011 Jan;12(1):96-104. (PMID: 21151104) ; J Immunol. 2003 Dec 1;171(11):6173-7. (PMID: 14634133) ; Cell. 2012 Oct 12;151(2):289-303. (PMID: 23021777) ; Int Immunol. 2011 Nov;23(11):701-12. (PMID: 21937456) ; Science. 2005 Jan 21;307(5708):430-3. (PMID: 15662016) ; Cell. 2000 Mar 17;100(6):655-69. (PMID: 10761931) ; Immunity. 2009 Apr 17;30(4):576-87. (PMID: 19362022) ; Proc Natl Acad Sci U S A. 2008 Jul 15;105(28):9721-6. (PMID: 18607004) ; PLoS One. 2013;8(2):e57379. (PMID: 23460846) ; Microbes Infect. 2004 May;6(6):529-35. (PMID: 15158185) ; Immunity. 2015 Mar 17;42(3):499-511. (PMID: 25769610) ; Trends Immunol. 2016 Jan;37(1):17-31. (PMID: 26700314) ; J Immunol. 2007 Jan 1;178(1):605-12. (PMID: 17182601) ; Nucl Recept Signal. 2009;7:e003. (PMID: 19381306) ; Arthritis Rheum. 2009 Feb;60(2):390-5. (PMID: 19180498) ; Eur J Immunol. 2016 Jun;46(6):1404-14. (PMID: 27067635) ; Immunol Rev. 2008 Jun;223:87-113. (PMID: 18613831) ; Arthritis Rheum. 2012 Jan;64(1):162-72. (PMID: 21905017) Contributed Indexing: Keywords: AHR; IL-17; T-bet over-expression Substance Nomenclature: 0 (Interleukin-6) ; 0 (Receptors, Aryl Hydrocarbon) ; 0 (STAT3 Transcription Factor) ; 0 (T-Box Domain Proteins) ; 0 (T-box transcription factor TBX21) ; 82115-62-6 (Interferon-gamma) Entry Date(s): Date Created: 20161210 Date Completed: 20170508 Latest Revision: 20181113 Update Code: 20240513 PubMed Central ID: PMC5343350

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T-bet over-expression regulates aryl hydrocarbon receptor-mediated T helper type 17 differentiation through an interferon (IFN)γ-independent pathway.