The contribution of genetic variation and infection to the pathogenesis of ANCA-associated systemic vasculitis
Open Access
- 1 January 2010
- journal article
- review article
- Published by Springer Nature in Arthritis Research & Therapy
- Vol. 12 (1) , 202
- https://doi.org/10.1186/ar2928
Abstract
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.Keywords
This publication has 99 references indexed in Scilit:
- Confirmation of the genetic association of CTLA4 and PTPN22 with ANCA-associated vasculitisBMC Medical Genetics, 2009
- Contrasting genetic association of IL2RAwith SLE and ANCA – associated vasculitisBMC Medical Genetics, 2009
- An integrated approach for measuring copy number variation at theFCGR3(CD16) locusHuman Mutation, 2009
- DNAM-1 promotes activation of cytotoxic lymphocytes by nonprofessional antigen-presenting cells and tumorsThe Journal of Experimental Medicine, 2008
- Molecular mimicry in pauci-immune focal necrotizing glomerulonephritisNature Medicine, 2008
- Copy number of FCGR3B, which is associated with systemic lupus erythematosus, correlates with protein expression and immune complex uptakeThe Journal of Experimental Medicine, 2008
- Copy-number variation and association studies of human diseaseNature Genetics, 2007
- Gene Copy-Number Variation and Associated Polymorphisms of Complement Component C4 in Human Systemic Lupus Erythematosus (SLE): Low Copy Number Is a Risk Factor for and High Copy Number Is a Protective Factor against SLE Susceptibility in European AmericansAmerican Journal of Human Genetics, 2007
- FCGR3B copy number variation is associated with susceptibility to systemic, but not organ-specific, autoimmunityNature Genetics, 2007
- Complexes between proteinase 3, α1‐antitrypsin and proteinase 3 anti‐neutrophil cytoplasm autoantibodies: a comparison between α1‐antitrypsin PiZ allele carriers and non‐carriers with Wegener's granulomatosisEuropean Journal of Clinical Investigation, 1996