期刊
FRONTIERS IN IMMUNOLOGY
卷 5, 期 -, 页码 1-13出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2014.00248
关键词
hepatitis C; mixed cryoglobulinemia; vasculitis; interferon-stimulated genes
类别
资金
- intramural program of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, Bethesda, MD, USA
This study examines the distinct gene expression profile of peripheral blood mononuclear cells from patients with chronic hepatitis C infection and mixed cryoglobulinemic (MC) vasculitis. Our DNA microarray analysis indicates that hepatitis C virus (HCV)-associated MC vasculitis is characterized by compromised neutrophil function, impaired chemotaxis, and increased interferon-stimulated gene (ISG) expression, contributing to overall MC pathogenesis and end-organ damage. Increased ISG expression is suggestive of an enhanced endogenous interferon gene signature. PBMC depletion assays demonstrate that this increased expression is likely due to an activation of monocytes and not a direct result of B cell expansion. Notably, this monocyte activation of ISG expression in HCV-associated MC vasculitis suggests a poor predictor status of interferon-based treatment. Further analysis of PBMC gene expression profiles before and after in vivo B cell depletion therapy is critical to completely understanding the mechanisms of MC vasculitis pathogenesis.
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