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Highly polarized T h17 cells induce EAE via a T ‐bet independent mechanism

dc.contributor.authorGrifka‐walk, Heather M.en_US
dc.contributor.authorLalor, Stephen J.en_US
dc.contributor.authorSegal, Benjamin M.en_US
dc.date.accessioned2013-12-04T18:57:33Z
dc.date.available2015-01-05T13:54:43Zen_US
dc.date.issued2013-11en_US
dc.identifier.citationGrifka‐walk, Heather M. ; Lalor, Stephen J.; Segal, Benjamin M. (2013). "Highly polarized T h17 cells induce EAE via a T â bet independent mechanism." European Journal of Immunology 43(11): 2824-2831.en_US
dc.identifier.issn0014-2980en_US
dc.identifier.issn1521-4141en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/101823
dc.publisherWiley Periodicals, Inc.en_US
dc.subject.otherMultiple Sclerosisen_US
dc.subject.otherT H17 Cellsen_US
dc.subject.otherT ‐Beten_US
dc.subject.otherExperimental Autoimmune Encephalomyelitisen_US
dc.subject.otherNeuroimmunologyen_US
dc.titleHighly polarized T h17 cells induce EAE via a T ‐bet independent mechanismen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelBiological Chemistryen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/101823/1/eji2739-sup-0001-FigureS1.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/101823/2/eji2739-sup-0001-FigS1.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/101823/3/eji2739-sup-0002-S1.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/101823/4/eji2739-sup-0002-PRC.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/101823/5/eji2739.pdf
dc.identifier.doi10.1002/eji.201343723en_US
dc.identifier.sourceEuropean Journal of Immunologyen_US
dc.identifier.citedreferenceBettelli, E., Sullivan, B., Szabo, S. J., Sobel, R. A., Glimcher, L. H. and Kuchroo, V. K., Loss of T ‐bet, but not STAT 1, prevents the development of experimental autoimmune encephalomyelitis. J. Exp. Med. 2004. 200: 79 – 87.en_US
dc.identifier.citedreferenceFerber, I. A., Brocke, S., Taylor‐Edwards, C., Ridgway, W., Dinisco, C., Steinman, L., Dalton, D. and Fathman, C. G., Mice with a disrupted IFN ‐gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis ( EAE ). J. Immunol. 1996. 156: 5 – 7.en_US
dc.identifier.citedreferenceHaak, S., Croxford, A. L., Kreymborg, K., Heppner, F. L., Pouly, S., Becher, B. and Waisman, A., IL ‐17 A and IL ‐17 F do not contribute vitally to autoimmune neuro‐inflammation in mice. J. Clin. Invest. 2009. 119: 61 – 69.en_US
dc.identifier.citedreferenceKroenke, M. A., Chensue, S. W. and Segal, B. M., EAE mediated by a non‐ IFN ‐γ/non‐ IL ‐17 pathway. Eur. J. Immunol. 2010. 40: 2340 – 2348.en_US
dc.identifier.citedreferenceYang, Y., Weiner, J., Liu, Y., Smith, A. J., Huss, D. J., Winger, R., Peng, H. et al., T ‐bet is essential for encephalitogenicity of both T h1 and T h17 cells. J. Exp. Med. 2009. 206: 1549 – 1564.en_US
dc.identifier.citedreferenceMullen, A. C., High, F. A., Hutchins, A. S., Lee, H. W., Villarino, A. V., Livingston, D. M., Kung, A. L. et al., Role of T ‐bet in commitment of TH 1 cells before IL ‐12‐dependent selection. Science 2001. 292: 1907 – 1910.en_US
dc.identifier.citedreferenceSzabo, S. J., Kim, S. T., Costa, G. L., Zhang, X., Fathman, C. G. and Glimcher, L. H., A novel transcription factor, T ‐bet, directs T h1 lineage commitment. Cell 2000. 100: 655 – 669.en_US
dc.identifier.citedreferenceGocke, A. R., Cravens, P. D., Ben, L. H., Hussain, R. Z., Northrop, S. C., Racke, M. K. and Lovett‐Racke, A. E., T ‐bet regulates the fate of T h1 and T h17 lymphocytes in autoimmunity. J. Immunol. 2007. 178: 1341 – 1348.en_US
dc.identifier.citedreferenceLee, Y. K., Turner, H., Maynard, C. L., Oliver, J. R., Chen, D., Elson, C. O. and Weaver, C. T., Late developmental plasticity in the T helper 17 lineage. Immunity 2009. 30: 92 – 107.en_US
dc.identifier.citedreferenceLexberg, M. H., Taubner, A., Förster, A., Albrecht, I., Richter, A., Kamradt, T., Radbruch, A. and Chang, H. D., Th memory for interleukin‐17 expression is stable in vivo. Eur. J. Immunol. 2008. 38: 2654 – 2664.en_US
dc.identifier.citedreferenceMukasa, R., Balasubramani, A., Lee, Y. K., Whitley, S. K., Weaver, B. T., Shibata, Y., Crawford, G. E. et al., Epigenetic instability of cytokine and transcription factor gene loci underlies plasticity of the T helper 17 cell lineage. Immunity 2010. 32: 616 – 627.en_US
dc.identifier.citedreferenceHirota, K., Duarte, J. H., Veldhoen, M., Hornsby, E., Li, Y., Cua, D. J., Ahlfors, H. et al., Fate mapping of IL ‐17‐producing T cells in inflammatory responses. Nat. Immunol. 2011. 12: 255 – 263.en_US
dc.identifier.citedreferenceKurschus, F. C., Croxford, A. L., Heinen, A. P., Wörtge, S., Ielo, D. and Waisman, A., Genetic proof for the transient nature of the T h17 phenotype. Eur. J. Immunol. 2010. 40: 3336 – 3346.en_US
dc.identifier.citedreferenceLovett‐Racke, A. E., Rocchini, A. E., Choy, J., Northrop, S. C., Hussain, R. Z., Ratts, R. B., Sikder, D. and Racke, M. K., Silencing T ‐bet defines a critical role in the differentiation of autoreactive T lymphocytes. Immunity 2004. 21: 719 – 731.en_US
dc.identifier.citedreferenceFrisullo, G., Angelucci, F., Caggiula, M., Nociti, V., Iorio, R., Patanella, A. K., Sancricca, C. et al., p STAT 1, p STAT 3, and T ‐bet expression in peripheral blood mononuclear cells from relapsing‐remitting multiple sclerosis patients correlates with disease activity. J. Neurosci. Res. 2006. 84: 1027 – 1036.en_US
dc.identifier.citedreferenceNath, N., Prasad, R., Giri, S., Singh, A. K. and Singh, I., T ‐bet is essential for the progression of experimental autoimmune encephalomyelitis. Immunology 2006. 118: 384 – 391.en_US
dc.identifier.citedreferenceMuranski, P., Borman, Z. A., Kerkar, S. P., Klebanoff, C. A., Ji, Y., Sanchez‐Perez, L., Sukumar, M. et al., T h17 cells are long lived and retain a stem cell‐like molecular signature. Immunity 2011. 35: 972 – 985.en_US
dc.identifier.citedreferenceDuhen, R., Glatigny, S., Arbelaez, C. A., Blair, T. C., Oukka, M. and Bettelli, E., Cutting edge: the pathogenicity of IFN ‐gamma‐producing T h17 cells is independent of T ‐bet. J. Immunol. 2013. 190: 4478 – 4482.en_US
dc.identifier.citedreferenceKing, I. L., Dickendesher, T. L. and Segal, B. M., Circulating L y‐6 C + myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood 2009. 113: 3190 – 3197.en_US
dc.identifier.citedreferenceEl‐Behi, M., Ciric, B., Dai, H., Yan, Y., Cullimore, M., Safavi, F., Zhang, G. X. et al., The encephalitogenicity of T ( H )17 cells is dependent on IL ‐1‐ and IL ‐23‐induced production of the cytokine GM ‐ CSF. Nat. Immunol. 2011. 12: 568 – 575.en_US
dc.identifier.citedreferenceCodarri, L., Gyülvészi, G., Tosevski, V., Hesske, L., Fontana, A., Magnenat, L., Suter, T. and Becher, B., ROR γt drives production of the cytokine GM ‐ CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation. Nat. Immunol. 2011. 12: 560 – 567.en_US
dc.identifier.citedreferenceCarlson, T., Kroenke, M., Rao, P., Lane, T. E. and Segal, B., The T h17‐ ELR + CXC chemokine pathway is essential for the development of central nervous system autoimmune disease. J. Exp. Med. 2008. 205: 811 – 823.en_US
dc.identifier.citedreferenceLord, G. M., Rao, R. M., Choe, H., Sullivan, B. M., Lichtman, A. H., Luscinskas, F. W. and Glimcher, L. H., T ‐bet is required for optimal proinflammatory CD 4+ T ‐cell trafficking. Blood 2005. 106: 3432 – 3439.en_US
dc.identifier.citedreferenceKroenke, M. A., Carlson, T. J., Andjelkovic, A. V. and Segal, B. M., IL ‐12‐ and IL ‐23‐modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition. J. Exp. Med. 2008. 205: 1535 – 1541.en_US
dc.identifier.citedreferenceAxtell, R. C., de Jong, B. A., Boniface, K., van der Voort, L. F., Bhat, R., De Sarno, P., Naves, R. et al., T helper type 1 and 17 cells determine efficacy of interferon‐beta in multiple sclerosis and experimental encephalomyelitis. Nat. Med. 2010. 16: 406 – 412.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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