pubmed-article:16027240 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C0024141 | lld:lifeskim |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C0004358 | lld:lifeskim |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C0963057 | lld:lifeskim |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:16027240 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:16027240 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:16027240 | pubmed:dateCreated | 2005-7-19 | lld:pubmed |
pubmed-article:16027240 | pubmed:abstractText | Systemic autoimmune disease in humans and mice is characterized by loss of immunologic tolerance to a restricted set of self-nuclear antigens. Autoantigens, such as double-stranded (ds) DNA and the RNA-containing Smith antigen (Sm), may be selectively targeted in systemic lupus erythematosus because of their ability to activate a putative common receptor. Toll-like receptor 9 (TLR9), a receptor for CpG DNA, has been implicated in the activation of autoreactive B cells in vitro, but its role in promoting autoantibody production and disease in vivo has not been determined. We show that in TLR9-deficient lupus-prone mice, the generation of anti-dsDNA and antichromatin autoantibodies is specifically inhibited. Other autoantibodies, such as anti-Sm, are maintained and even increased in TLR9-deficient mice. In contrast, ablation of TLR3, a receptor for dsRNA, did not inhibit the formation of autoantibodies to either RNA- or DNA-containing antigens. Surprisingly, we found that despite the lack of anti-dsDNA autoantibodies in TLR9-deficient mice, there was no effect on the development of clinical autoimmune disease or nephritis. These results demonstrate a specific requirement for TLR9 in autoantibody formation in vivo and indicate a critical role for innate immune activation in autoimmunity. | lld:pubmed |
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pubmed-article:16027240 | pubmed:language | eng | lld:pubmed |
pubmed-article:16027240 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16027240 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16027240 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16027240 | pubmed:month | Jul | lld:pubmed |