View Item 

Show simple item record

Interleukin-17-producing γδ + T cells protect NOD mice from type 1 diabetes through a mechanism involving transforming growth factor-β

dc.contributor.authorWang, Renxien_US
dc.contributor.authorChen, Guojiangen_US
dc.contributor.authorWang, Jiananen_US
dc.contributor.authorXu, Ruonanen_US
dc.contributor.authorWang, Liyanen_US
dc.contributor.authorHan, Genchengen_US
dc.contributor.authorFeng, Jiannanen_US
dc.contributor.authorLi, Xiaen_US
dc.contributor.authorGuo, Renfengen_US
dc.contributor.authorFu, Lien_US
dc.contributor.authorShen, Beifenen_US
dc.contributor.authorLi, Yanen_US
dc.date.accessioned2010-06-01T21:57:31Z
dc.date.available2010-06-01T21:57:31Z
dc.date.issued2010-02en_US
dc.identifier.citationHan, Gencheng; Wang, Renxi; Chen, Guojiang; Wang, Jianan; Xu, Ruonan; Wang, Liyan; Feng, Jiannan; Li, Xia; Guo, Renfeng; Fu, Li; Shen, Beifen; Li, Yan (2010). "Interleukin-17-producing γδ + T cells protect NOD mice from type 1 diabetes through a mechanism involving transforming growth factor-β." Immunology 129(2): 197-206. <http://hdl.handle.net/2027.42/74990>en_US
dc.identifier.issn0019-2805en_US
dc.identifier.issn1365-2567en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/74990
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=19824917&dopt=citationen_US
dc.format.extent482475 bytes
dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherBlackwell Publishing Ltden_US
dc.rightsJournal compilation © 2010 Blackwell Publishing Ltden_US
dc.subject.otherAutoimmune Diabetesen_US
dc.subject.otherInterleukin-17en_US
dc.subject.otherNon-obese Diabetic (NOD)en_US
dc.subject.otherTransforming Growth Factor-βen_US
dc.subject.otherγδ T Cellsen_US
dc.titleInterleukin-17-producing γδ + T cells protect NOD mice from type 1 diabetes through a mechanism involving transforming growth factor-βen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelMicrobiology and Immunologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherDepartment of Molecular Immunology, Institute of Basic Medical Sciences, Beijing, Chinaen_US
dc.contributor.affiliationotherLaboratory of Cellular and Molecular Immunology, Henan University, Kaifeng, Chinaen_US
dc.contributor.affiliationotherDepartment of Breast Pathology, Tianjin Medical University Cancer Hospital, Tianjin, Chinaen_US
dc.identifier.pmid19824917en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/74990/1/j.1365-2567.2009.03166.x.pdf
dc.identifier.doi10.1111/j.1365-2567.2009.03166.xen_US
dc.identifier.sourceImmunologyen_US
dc.identifier.citedreferenceAnderson MS, Bluestone JA. The NOD mouse: a model of immune dysregulation. Annu Rev Immunol 2005; 23: 447 – 85.en_US
dc.identifier.citedreferenceSavinov AY, Wong FS, Chervonsky AV. IFN-g affects the homing of diabetogenic T cells. J Immunol 2001; 167: 6637 – 43.en_US
dc.identifier.citedreferenceHan G, Li Y, Wang J et al. Active tolerance induction and prevention of autoimmune diabetes by immunogene therapy using recombinant adenoassociated virus expressing glutamic acid decarboxylase 65 peptide GAD (500-585). J Immunol 2005; 174: 4516 – 24.en_US
dc.identifier.citedreferenceCooke A, Phillips JM, Parish NM. Tolerogenic strategies to halt or prevent type 1 diabetes. Nat Immunol 2001; 2: 810.en_US
dc.identifier.citedreferencePark H, Li Z, Yang XO et al. A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat Immunol 2005; 6: 1133 – 41.en_US
dc.identifier.citedreferenceNakae S, Nambu A, Sudo K, Iwakura Y. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol 2003; 171: 6173 – 7.en_US
dc.identifier.citedreferenceCua DJ, Sherlock J, Chen Y et al. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature 2003; 421: 744 – 8.en_US
dc.identifier.citedreferenceHashimoto T, Akiyama K, Kobayashi N, Mori A. Comparison of IL-17 production by helper T cells among atopic and nonatopic asthmatics and control subjects. Int Arch Allergy Immunol 2005; 137: 51 – 4.en_US
dc.identifier.citedreferenceBending D, De La Pea H, Veldhoen M, Phillips JM, Uyttenhove C, Stockinger B, Cooke A. Highly purified Th17 cells from BDC2·5NOD mice convert into Th1-like cells in NOD/SCID recipient mice. J Clin Invest 2009, doi: 10.1172/JCI37865.en_US
dc.identifier.citedreferenceMartin-Orozco N, Chung Y, Chang SH, Wang YH, Dong C. Th17 cells promote pancreatic inflammation but only induce diabetes efficiently in lymphopenic hosts after conversion into Th1 cells. Eur J Immunol 2009; 39: 216 – 24.en_US
dc.identifier.citedreferenceLockhart E, Green AM, Flynn JL. IL-17 production is dominated by γδT cells rather than CD4 T cells during Mycobacterium tuberculosis infection. J Immunol 2006; 177: 4662 – 9.en_US
dc.identifier.citedreferenceShibata K, Yamada H, Hara H, Kishihara K, Yoshikai Y. Resident Vγ1γδT cells control early infiltration of Neutrophils after Escherichia coli infection via IL-17 production. J Immunol 2007; 178: 4466 – 72.en_US
dc.identifier.citedreferenceBhagat G, Naiyer AJ, Shah JG, Harper J, Jabri B, Wang TC, Green PH, Manavalan JS. Small intestinal CD8+TCRγδ+NKG2A+ intraepithelial lymphocytes have attributes of regulatory cells in patients with celiac disease. J Clin Invest 2008; 118: 281 – 93.en_US
dc.identifier.citedreferenceHarrison LC, DempseyCollier M, Kramer DR, Takahashi K. Aerosol insulin induces regulatory CD8 gd T cells that prevent murine insulin-dependent diabetes. J Exp Med 1996; 184: 2167 – 74.en_US
dc.identifier.citedreferenceSeo N, Tokura Y, Takigawa M, Egawa K. Depletion of IL-10- and TGF-b-producing regulatory gd T cells by administering a daunomycin -conjugated specific monoclonal antibody in early tumor lesions augments the activity of CTLs and NK cells. J Immunol 1999; 163: 242 – 9.en_US
dc.identifier.citedreferenceLocke NR, Stankovic S, Funda DP, Harrison LC. TCR gd intraepithelial lymphocytes are required for self-tolerance. J Immunol 2006; 176: 6553 – 9.en_US
dc.identifier.citedreferenceNagaeva O, Jonsson L, Mincheva-Nilsson L. Dominant IL-10 and TGF-b mRNA expression in gdT cells of human early pregnancy decidua suggests immunoregulatory potential. Am J Reprod Immunol 2002; 48: 9 – 17.en_US
dc.identifier.citedreferencePeng G, Wang H, Peng W, Kiniwa Y, Seo KH, Wang R. Tumor-infiltrating gammadelta T cells suppress T and dendritic cell function via mechanisms controlled by a unique Toll-like receptor signaling pathway. Immunity 2007; 27: 334 – 48.en_US
dc.identifier.citedreferenceTschÖp J, Martignoni A, Goetzman HS, et al. gdT cells mitigate the organ injury and mortality of sepsis. J Leukoc Biol. 2008; 83: 1 – 8.en_US
dc.identifier.citedreferenceCarding SR, Egan PJ. γδT cells: functional plasticity and heterogeneity. Nat Rev Immunol 2002; 2: 336 – 45.en_US
dc.identifier.citedreferenceKohyama S, Ohno S, Isoda A et al. IL-23 enhances host defense against Vaccinia virus infection via a mechanism partly involving IL-17. J Immunol 2007; 179: 3917 – 25.en_US
dc.identifier.citedreferenceYu S, Sharp GC, Braley-Mullen H. TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma deficient NOD.H-2h4 Mice. J Immunol, 2008; 181: 2238 – 45.en_US
dc.identifier.citedreferenceNakae S, Iwakura Y, Suto H, Galli SJ. Phenotypic differences between Th1 and Th17 cells and negative regulation of Th1 cell differentiation by IL-17. J Leukoc Biol 2007; 81: 1258 – 68.en_US
dc.identifier.citedreferenceHarrington LE, Hatton RD, Mangan PR, Turner H, Murphy TL, Murphy KM, Weaver CT. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat Immunol 2005; 6: 1123 – 32.en_US
dc.identifier.citedreferenceLangrish CL, Chen Y, Blumenschein WM et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med 2005; 201: 233 – 40.en_US
dc.identifier.citedreferenceKorn T, Reddy J, Gao W et al. Myelin-specific regulatory T cells accumulate in the CNS but fail to control autoimmune inflammation. Nat Med 2007; 13: 4.en_US
dc.identifier.citedreferenceRoark CL, Simonian PL, Fontenot AP, Born WB, O`Brien RL. Gamma delta T cells: an important source of IL-17. Curr Opin Immunol 2008; 20: 1 – 5.en_US
dc.identifier.citedreferenceCheng L, Cui Y, Shao H et al. Mouse γδ T cells are capable of expressing MHC class II molecules, and of functioning as antigen-presenting cells. J Neuroimmunol 2008; 203: 3 – 11.en_US
dc.identifier.citedreferenceThedrez A, Sabourin C, Gertner J, Devilder MC, Allain-Maillet S, FourniÉ JJ, Scotet E, Bonneville M. Self/non-self discrimination by gammadelta T cells: simple solutions for a complex. Immunol Rev 2007; 215: 123 – 35.en_US
dc.identifier.citedreferenceRoark CL, French JD, Taylor MA, Bendele AM, Born WK, O’Brien RL. Exacerbation of collagen-induced arthritis by oligoclonal, IL-17-producing gamma delta T cells. J Immunol 2007; 179: 5576 – 83.en_US
dc.identifier.citedreferenceRomani L, Fallarino F, De Luca A et al. Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease. Nature 2008; 451: 211 – 5.en_US
dc.identifier.citedreferenceMcGeachy MJ, Bak-Jensen KS, Chen Y, Tato CM, Blumenschein W, McClanahan T, Cua DJ. TGF-b and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell–mediated pathology. Nat Immun 2007; 8: 12.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
j.1365-2567.2009.03166.x.pdf
Size:
471.1KB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.