| pubmed-article:16580840 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16580840 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
| pubmed-article:16580840 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:16580840 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:16580840 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:16580840 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:16580840 | pubmed:dateCreated | 2006-5-8 | lld:pubmed |
| pubmed-article:16580840 | pubmed:abstractText | It has long been established that type 1 diabetes (T1D) is a T cell-mediated autoimmune disease, with CD4+ and CD8+ T cells being largely responsible for the destruction of beta cells within the pancreatic islets of Langerhans. Although autoantibodies specific for islet cell proteins are regularly detected in individuals with T1D and can be utilized as effective markers for predicting the onset of disease, they are not believed to be directly pathogenic to beta cells. Thus, activation of autoantibody-secreting B cells has long been regarded as a secondary consequence of the ongoing self-reactive T cell response. However, recently, studies in the nonobese diabetic mouse model of disease have demonstrated that B cells are an important component in the development of T1D by virtue of their ability to act as the preferential antigen presenting cell population required for efficient expansion of diabetogenic CD4+ T cells. Furthermore, autoantibodies might also be responsible for mediating early beta cell pathogenesis in this model. | lld:pubmed |
| pubmed-article:16580840 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16580840 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16580840 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16580840 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16580840 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16580840 | pubmed:issn | 1043-2760 | lld:pubmed |
| pubmed-article:16580840 | pubmed:author | pubmed-author:GreyShane TST | lld:pubmed |
| pubmed-article:16580840 | pubmed:author | pubmed-author:SilveiraPablo... | lld:pubmed |
| pubmed-article:16580840 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16580840 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:16580840 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16580840 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16580840 | pubmed:pagination | 128-35 | lld:pubmed |
| pubmed-article:16580840 | pubmed:dateRevised | 2009-9-28 | lld:pubmed |
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| pubmed-article:16580840 | pubmed:meshHeading | pubmed-meshheading:16580840... | lld:pubmed |
| pubmed-article:16580840 | pubmed:articleTitle | B cells in the spotlight: innocent bystanders or major players in the pathogenesis of type 1 diabetes. | lld:pubmed |
| pubmed-article:16580840 | pubmed:affiliation | Immunology and Inflammation Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia. p.silveira@garvan.org.au | lld:pubmed |
| pubmed-article:16580840 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16580840 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:16580840 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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