期刊
BLOOD
卷 116, 期 11, 页码 1951-1957出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-03-274605
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资金
- Swedish Research Council
- Medical Faculty at Lund University
- Alfred Osterlund's Foundation
- Crafoord Foundation
- Greta and Johan Kock's Foundation
- King Gustaf V's 80th Birthday Foundation
- Lund University Hospital
- Swedish Rheumatism Association
- Swedish Society of Medicine
- Foundation of the National Board of Health and Welfare
Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in patients with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (P<.0001) were found to be up-regulated in platelets from SLE patients compared with healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFN alpha that up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE. (Blood. 2010; 116(11): 1951-1957)
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