| pubmed-article:20236493 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20236493 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:20236493 | lifeskim:mentions | umls-concept:C0264939 | lld:lifeskim |
| pubmed-article:20236493 | lifeskim:mentions | umls-concept:C0042333 | lld:lifeskim |
| pubmed-article:20236493 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
| pubmed-article:20236493 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:20236493 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20236493 | pubmed:dateCreated | 2010-5-18 | lld:pubmed |
| pubmed-article:20236493 | pubmed:abstractText | The aetiology of anti-neutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis has not been well defined. Here we review two factors which may play a role in the pathogenesis of the disease: genetics and infection. In particular, we discuss the role of autoantibodies to LAMP-2, which may arise following infection with Gram-negative bacteria, and may contribute to the development of ANCA-associated systemic vasculitis in genetically susceptible individuals. | lld:pubmed |
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