期刊
RHEUMATOLOGY
卷 50, 期 6, 页码 1064-1069出版社
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keq459
关键词
Systemic lupus erythematosus; Growth arrest-specific protein 6; Axl; Receptor tyrosine kinase; Vitamin K; Inflammation; Autoimmunity
类别
资金
- Swedish government funds for clinical research (ALF)
- University hospital in Lund and Malmo
- Swedish Research Council [07143, 2008-2201]
- Wallenberg Foundation
- Osterlund's Foundation
- Medical Faculty at Lund University
- 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
Objectives. SLE is a systemic autoimmune disease with an annual incidence of 3.8 per 100 000. Several pathogenic mechanisms are believed to be operating in SLE, including an impaired clearance of apoptotic cells, activation of the type I IFN pathway and generation of autoimmune leucocytes. Growth arrest-specific protein 6 (Gas6) and its receptor Axl are known to regulate inflammation and may be implicated in lupus pathogenesis. We have recently developed immunological methods to quantify the vitamin-K-dependent protein Gas6 and its soluble receptor sAxl in human plasma, which we have used to investigate the role of Gas6 and soluble Axl in SLE. Methods. We have investigated the relation between the plasma concentrations of Gas6 and sAxl and disease activity and specific symptoms in 96 SLE patients. Results. Gas6 and sAxl concentrations correlated with SLEDAI (r = 0.48, P < 0.001 and r = 0.39, P < 0.001, respectively). Furthermore, concentrations of Gas6 and sAxl correlated with ESR and CRP and inversely with haemoglobin levels. Gas6 and sAxl concentrations were significantly higher in patients with anti-DNA antibodies, leucopenia and GN. Conclusion. The plasma concentrations of Gas6 and sAxl vary with disease activity in SLE, in particular GN, and may have a role in lupus pathogenesis. Furthermore, Gas6 and sAxl may be of use as biomarkers of disease activity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据