期刊
AUTOIMMUNITY
卷 43, 期 1, 页码 17-22出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/08916930903374832
关键词
Lupus T cells; epigenetics; DNA methylation; extracellular signal-regulated kinase pathway signaling; Protein Kinase delta
类别
资金
- PHS [AR42525, AG25877, ES015214]
- Department of Veterans Affairs
Systemic lupus erythematosus is a poorly understood autoimmune disease, characterized by autoantibodies to nuclear antigens and immune complex deposition in organs like the kidney. Current evidence indicates that a pathologic CD4+T cell subset, characterized by impaired extracellular signal-regulated kinase (ERK) pathway signaling, DNA hypomethylation, and consequent aberrant gene expression contributes to disease pathogenesis. Hydralazine is a lupus-inducing drug that also decreases T cell DNA methylation by inhibiting the ERK signaling pathway, replicating the defect found in lupus T cells. These observations suggest that defective ERK pathway signaling alters gene expression in T cells by inhibiting DNA methylation, contributing to lupus pathogenesis. The signaling defect in hydralazine-treated and lupus T cells has now been mapped to protein kinase C delta. Understanding the mechanism causing decreased ERK pathway signaling in lupus may shed light on mechanisms contributing to disease development in genetically predisposed people.
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