Abstract
By proteomic screening of sera obtained from patients with rheumatoid arthritis (RA), we previously identified leucine rich α2 glycoprotein (LRG) as a possible marker for inflammation. Unlike C-reactive protein (CRP), a biomarker widely used to evaluate inflammation, LRG is induced not only by IL-6 but also by other proinflammatory cytokines. In addition, LRG is upregulated not only in liver but also in local inflammatory sites. Therefore, serum LRG is a novel inflammatory marker applicable to evaluate inflammation in many diseases including ulcerative colitis in which serum CRP often fails to reflect disease activity and RA to which IL-6-blocking biologic agents such as tocilizumab are given as a first line therapy. Interestingly, evidence indicates that LRG is functionally involved in pathogenesis of inflammation, by promoting cellular proliferation, differentiation and angiogenesis via modulating TGF-β signaling.
Highlights
Whereas biologic agents targeting cytokines have shown great efficacy in treating diseases such as rheumatoid arthritis (RA) and inflammatory bowel disease, they still have several problems
By proteomic screening of sera obtained from patients with rheumatoid arthritis (RA), we previously identified leucine rich a2 glycoprotein (LRG) as a possible marker for inflammation
Serum LRG is a novel inflammatory marker applicable to evaluate inflammation in many diseases including ulcerative colitis in which serum C-reactive protein (CRP) often fails to reflect disease activity and RA to which IL-6-blocking biologic agents such as tocilizumab are given as a first line therapy
Summary
Whereas biologic agents targeting cytokines have shown great efficacy in treating diseases such as rheumatoid arthritis (RA) and inflammatory bowel disease, they still have several problems. When patients receive IL-6-blocking agents such as tocilizumab, inflammatory markers CRP and SAA do not elevate even at disease flares [2]. This causes a serious problem in evaluating efficacy of biologic agents during therapy. When patients receiving these agents develop infection such as pneumonia and tuberculosis, current markers such as CRP and SAA are unable to reflect inflammation. This raises another serious problem in detection of concomitant infection, a major adverse effect of biologic agents. Marker reflecting disease activity of RA better than CRP [3]
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