| pubmed-article:12707359 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12707359 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
| pubmed-article:12707359 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:12707359 | lifeskim:mentions | umls-concept:C0017260 | lld:lifeskim |
| pubmed-article:12707359 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
| pubmed-article:12707359 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
| pubmed-article:12707359 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:12707359 | pubmed:dateCreated | 2003-4-22 | lld:pubmed |
| pubmed-article:12707359 | pubmed:abstractText | Since the basic mechanisms behind the beneficial effects of IFN-beta in multiple sclerosis (MS) patients are still obscure, here we have investigated the effects of IFN-beta gene disruption on the commonly used animal model for MS, experimental autoimmune encephalomyelitis (EAE). We show that IFN-beta knockout (KO) mice are more susceptible to EAE than their wild-type (wt) littermates; they develop more severe and chronic neurological symptoms with more extensive CNS inflammation and demyelination. However, there was no discrepancy observed between wt and KO mice regarding the capacity of T cells to proliferate or produce IFN-gamma in response to recall Ag. Consequently, we addressed the effect of IFN-beta on encephalitogenic T cell development and the disease initiation phase by passive transfer of autoreactive T cells from KO or wt littermates to both groups of mice. Interestingly, IFN-beta KO mice acquired a higher incidence and augmented EAE regardless of the source of T cells. This shows that the anti-inflammatory effect of endogenous IFN-beta is predominantly exerted on the effector phase of the disease. Histopathological investigations of CNS in the effector phase revealed an extensive microglia activation and TNF-alpha production in IFN-beta KO mice; this was virtually absent in wt littermates. This coincided with an increase in effector functions of T cells in IFN-beta KO mice, as measured by IFN-gamma and IL-4 production. We suggest that lack of endogenous IFN-beta in CNS leads to augmented microglia activation, resulting in a sustained inflammation, cytokine production, and tissue damage with consequent chronic neurological deficits. | lld:pubmed |
| pubmed-article:12707359 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12707359 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12707359 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12707359 | pubmed:month | May | lld:pubmed |
| pubmed-article:12707359 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:MattssonRagna... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:HolmdahlRikar... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:LeandersonTom... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:TreschowAlexa... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:Issazadeh-Nav... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:NavikasVaidri... | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:TeigeIngridI | lld:pubmed |
| pubmed-article:12707359 | pubmed:author | pubmed-author:TeigeAnnaA | lld:pubmed |
| pubmed-article:12707359 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12707359 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12707359 | pubmed:volume | 170 | lld:pubmed |
| pubmed-article:12707359 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12707359 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12707359 | pubmed:pagination | 4776-84 | lld:pubmed |
| pubmed-article:12707359 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12707359 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12707359 | pubmed:articleTitle | IFN-beta gene deletion leads to augmented and chronic demyelinating experimental autoimmune encephalomyelitis. | lld:pubmed |
| pubmed-article:12707359 | pubmed:affiliation | Section for Medical Inflammation Research, Department of Cell and Molecular Biology, University of Lund, Lund, Sweden. | lld:pubmed |
| pubmed-article:12707359 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12707359 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:12707359 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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