| pubmed-article:20348925 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C0026769 | lld:lifeskim |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C0014070 | lld:lifeskim |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C0015980 | lld:lifeskim |
| pubmed-article:20348925 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:20348925 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20348925 | pubmed:dateCreated | 2010-4-8 | lld:pubmed |
| pubmed-article:20348925 | pubmed:abstractText | Interferon-beta (IFN-beta) is the major treatment for multiple sclerosis. However, this treatment is not always effective. Here we have found congruence in outcome between responses to IFN-beta in experimental autoimmune encephalomyelitis (EAE) and relapsing-remitting multiple sclerosis (RRMS). IFN-beta was effective in reducing EAE symptoms induced by T helper type 1 (T(H)1) cells but exacerbated disease induced by T(H)17 cells. Effective treatment in T(H)1-induced EAE correlated with increased interleukin-10 (IL-10) production by splenocytes. In T(H)17-induced disease, the amount of IL-10 was unaltered by treatment, although, unexpectedly, IFN-beta treatment still reduced IL-17 production without benefit. Both inhibition of IL-17 and induction of IL-10 depended on IFN-gamma. In the absence of IFN-gamma signaling, IFN-beta therapy was ineffective in EAE. In RRMS patients, IFN-beta nonresponders had higher IL-17F concentrations in serum compared to responders. Nonresponders had worse disease with more steroid usage and more relapses than did responders. Hence, IFN-beta is proinflammatory in T(H)17-induced EAE. Moreover, a high IL-17F concentration in the serum of people with RRMS is associated with nonresponsiveness to therapy with IFN-beta. | lld:pubmed |
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| pubmed-article:20348925 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20348925 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20348925 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20348925 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20348925 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20348925 | pubmed:issn | 1546-170X | lld:pubmed |
| pubmed-article:20348925 | pubmed:author | pubmed-author:GaoL YLY | lld:pubmed |
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| pubmed-article:20348925 | pubmed:author | pubmed-author:PolmanChris... | lld:pubmed |
| pubmed-article:20348925 | pubmed:author | pubmed-author:KillesteinJoe... | lld:pubmed |
| pubmed-article:20348925 | pubmed:author | pubmed-author:NavesRodrigoR | lld:pubmed |
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| pubmed-article:20348925 | pubmed:author | pubmed-author:MairRobertR | lld:pubmed |
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| pubmed-article:20348925 | pubmed:author | pubmed-author:KatzLiatL | lld:pubmed |
| pubmed-article:20348925 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20348925 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:20348925 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20348925 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20348925 | pubmed:pagination | 406-12 | lld:pubmed |
| pubmed-article:20348925 | pubmed:dateRevised | 2011-11-4 | lld:pubmed |
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