{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T19:05:49Z","timestamp":1790622349596,"version":"4.1.0"},"reference-count":25,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2013,8,23]],"date-time":"2013-08-23T00:00:00Z","timestamp":1377216000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2013,11]]},"abstract":"In the MOG<\/jats:styled-content>35\u201355<\/jats:sub> induced EAE<\/jats:styled-content> model, autoreactive T<\/jats:styled-content>h17 cells that accumulate in the central nervous system acquire T<\/jats:styled-content>h1 characteristics via a T<\/jats:styled-content>\u2010bet dependent mechanism. It remains to be determined whether T<\/jats:styled-content>h17 plasticity and encephalitogenicity are causally related to each other. Here, we show that IL<\/jats:styled-content>\u201023 polarized T<\/jats:styled-content>\u2010bet\u2212\/\u2212<\/jats:sup> T<\/jats:styled-content>h17 cells are unimpaired in either activation or proliferation, and induce higher quantities of the chemokines RANTES<\/jats:styled-content> and CXCL<\/jats:styled-content>2 than WT T<\/jats:styled-content>h17 cells. Unlike their WT<\/jats:styled-content> counterparts, T<\/jats:styled-content>\u2010bet\u2212\/\u2212<\/jats:sup> T<\/jats:styled-content>h17 cells retain an IL<\/jats:styled-content>\u201017hi<\/jats:sup>IFN<\/jats:styled-content>\u2010\u03b3neg\u2010lo<\/jats:sup> cytokine profile following adoptive transfer into syngeneic hosts. This population of highly polarized T<\/jats:styled-content>h17 effectors is capable of mediating EAE<\/jats:styled-content>, albeit with a milder clinical course. It has previously been reported that the signature T<\/jats:styled-content>h1 and T<\/jats:styled-content>h17 effector cytokines, IFN<\/jats:styled-content>\u2010\u03b3 and IL<\/jats:styled-content>\u201017, are dispensable for the development of autoimmune demyelinating disease. The current study demonstrates that the \u201cmaster regulator\u201d transcription factor, T<\/jats:styled-content>\u2010bet, is also not universally required for encephalitogenicity. Our results contribute to a growing body of data showing heterogeneity of myelin\u2010reactive T<\/jats:styled-content> cells and the independent mechanisms they employ to inflict damage to central nervous system tissues, complicating the search for therapeutic targets relevant across the spectrum of individuals with multiple sclerosis.<\/jats:p>","DOI":"10.1002\/eji.201343723","type":"journal-article","created":{"date-parts":[[2013,7,23]],"date-time":"2013-07-23T06:14:47Z","timestamp":1374560087000},"page":"2824-2831","source":"Crossref","is-referenced-by-count":57,"title":["Highly polarized T<\/scp>h17 cells induce EAE<\/scp> via a T<\/scp>\u2010bet independent mechanism"],"prefix":"10.1002","volume":"43","author":[{"given":"Heather M.","family":"Grifka\u2010Walk","sequence":"first","affiliation":[{"name":"Holtom\u2010Garrett Program in Neuroimmunology and Multiple Sclerosis Center, Department of Neurology University of Michigan Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen J.","family":"Lalor","sequence":"additional","affiliation":[{"name":"Holtom\u2010Garrett Program in Neuroimmunology and Multiple Sclerosis Center, Department of Neurology University of Michigan Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin M.","family":"Segal","sequence":"additional","affiliation":[{"name":"Holtom\u2010Garrett Program in Neuroimmunology and Multiple Sclerosis Center, Department of Neurology University of Michigan Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,8,23]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20080159"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2110"},{"key":"e_1_2_7_4_1","doi-asserted-by":"crossref","first-page":"5","DOI":"10.4049\/jimmunol.156.1.5","article-title":"Mice with a disrupted IFN\u2010gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE)","volume":"156","author":"Ferber I. 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