Emily C. Baechler1, Franak Batliwalla1, George Karypis1, Patrick M. Gaffney1, Ward Ortmann1, Karl J. Espe1, Katherine B. Shark1, W. J. Grande1, Karis M. H. Hughes1, Vivek Kapur1, Peter K. Gregersen1, Timothy W. Behrens1
1Departments of Medicine, Computer Science and Engineering, and Veterinary Pathobiology, University of Minnesota, Minneapolis, MN 55455; and Center for Genomics and Human Genetics, North Shore Long Island Jewish Research Institute, Manhasset, NY 11030
Tóm tắt
Systemic lupus erythematosus (SLE) is a complex, inflammatory autoimmune disease that affects multiple organ systems. We used global gene expression profiling of peripheral blood mononuclear cells to identify distinct patterns of gene expression that distinguish most SLE patients from healthy controls. Strikingly, about half of the patients studied showed dysregulated expression of genes in the IFN pathway. Furthermore, this IFN gene expression “signature” served as a marker for more severe disease involving the kidneys, hematopoetic cells, and/or the central nervous system. These results provide insights into the genetic pathways underlying SLE, and identify a subgroup of patients who may benefit from therapies targeting the IFN pathway.
