Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a complex pathogenesis involving multiple genetic and environmental contributions. DNA microarray technology has recently been applied to unravel some of this complexity through genomewide profiling. Early studies using microarray analysis of peripheral blood mononuclear cells (PBMCs) from SLE patients revealed dysregulation of inflammatory cytokines, chemokines, and immune response-related genes, as well as genes involved in apoptosis, signal transduction, and the cell cycle. More recently, using arrays containing many more genes, 4 independent research groups have found that interferon (IFN)-regulated genes are highly overexpressed in the peripheral blood and kidney glomeruli of SLE patients, supporting a crucial role for interferon in SLE. Future studies focusing on target tissues or organs in lupus, including the kidney, may further contribute to our understanding of lupus pathogenesis while providing new targets for therapy.
|Number of pages||5|
|Issue number||7-8 SPEC.ISS.|
|State||Published - Nov 2004|
Bibliographical noteFunding Information:
Dr. Putterman is supported by NIH grants RO1 AR486912 and PO1 AI51392, a Target Identification in Lupus Award from the Alliance for Lupus Research/Arthritis Foundation and a Hulda Irene Duggan Arthritis Investigator Award from the Arthritis Foundation.
- DNA microarray
- Gene expression
- Systemic lupus erythematosus (SLE)