| pubmed-article:20620945 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20620945 | lifeskim:mentions | umls-concept:C0003864 | lld:lifeskim |
| pubmed-article:20620945 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:20620945 | lifeskim:mentions | umls-concept:C1014432 | lld:lifeskim |
| pubmed-article:20620945 | lifeskim:mentions | umls-concept:C0013126 | lld:lifeskim |
| pubmed-article:20620945 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:20620945 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:20620945 | pubmed:dateCreated | 2010-7-12 | lld:pubmed |
| pubmed-article:20620945 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20620945 | pubmed:abstractText | Commensal microbes can have a substantial impact on autoimmune disorders, but the underlying molecular and cellular mechanisms remain largely unexplored. We report that autoimmune arthritis was strongly attenuated in the K/BxN mouse model under germ-free (GF) conditions, accompanied by reductions in serum autoantibody titers, splenic autoantibody-secreting cells, germinal centers, and the splenic T helper 17 (Th17) cell population. Neutralization of interleukin-17 prevented arthritis development in specific-pathogen-free K/BxN mice resulting from a direct effect of this cytokine on B cells to inhibit germinal center formation. The systemic deficiencies of the GF animals reflected a loss of Th17 cells from the small intestinal lamina propria. Introduction of a single gut-residing species, segmented filamentous bacteria, into GF animals reinstated the lamina propria Th17 cell compartment and production of autoantibodies, and arthritis rapidly ensued. Thus, a single commensal microbe, via its ability to promote a specific Th cell subset, can drive an autoimmune disease. | lld:pubmed |
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| pubmed-article:20620945 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20620945 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20620945 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20620945 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20620945 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20620945 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:20620945 | pubmed:issn | 1097-4180 | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:LittmanDan... | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:BenoistChrist... | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:MathisDianeD | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:WuHsin-JungHJ | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:ShimaTatsuich... | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:UmesakiYoshin... | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:IvanovIvaylo... | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:HattoriKimieK | lld:pubmed |
| pubmed-article:20620945 | pubmed:author | pubmed-author:DarceJaimeJ | lld:pubmed |
| pubmed-article:20620945 | pubmed:copyrightInfo | Copyright 2010 Elsevier Inc. All rights reserved. | lld:pubmed |
| pubmed-article:20620945 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20620945 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:20620945 | pubmed:volume | 32 | lld:pubmed |
| pubmed-article:20620945 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20620945 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20620945 | pubmed:pagination | 815-27 | lld:pubmed |
| pubmed-article:20620945 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
| pubmed-article:20620945 | pubmed:meshHeading | pubmed-meshheading:20620945... | lld:pubmed |
| pubmed-article:20620945 | pubmed:meshHeading | pubmed-meshheading:20620945... | lld:pubmed |
| pubmed-article:20620945 | pubmed:meshHeading | pubmed-meshheading:20620945... | lld:pubmed |
