- Home
- Products
- Services
- Applications
- Resource
- Company
Glycobiology focuses on exploring the structure and biological functions of oligosaccharides and polysaccharides, and current research suggests that glycan chains are closely associated with various immune diseases, cardiovascular diseases, and tumors. Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by joint damage that leads to joint dysfunction and disability. At the same time, RA often affects the normal functioning of other tissues in patients, including the lungs, heart, and eyes. Cytokines are cellular molecules secreted by immune cells that are involved in messaging and stimulating cells to move toward sites of infection and trauma. In RA, cytokines are categorized as pro-inflammatory cytokines, joint inflammatory cytokines, anti-inflammatory cytokines, and natural cytokine antagonists.
Figure 1. The key factors that regulate osteoclast differentiation in rheumatoid arthritis. (McInnes I B, et al., 2007)
IL-1 is one of the most important pro-inflammatory cytokines that destroy articular cartilage in RA. IL-1 stimulates the expression of phospholipase A2 (PLA2) and cyclooxygenase-2 (COX-2) in human synoviocytes and promotes the synthesis and release of prostaglandins (PGE2) and collagenase in synoviocytes and chondrocytes, which leads to synoviocyte proliferation. In addition, IL-1 induces the synthesis of large amounts of metalloproteinase-collagen and matrix proteins in synovium and cartilage, further promoting proteoglycan production.
IL-6 plays a role in osteoclast differentiation, which can lead to bone destruction and mediate anemia caused by chronic inflammation. Thus, dysregulation of IL-6 expression is an important factor in the pathogenesis of RA. Many studies have shown that RA patients have high serum expression of IL-6. In the last decade, IL-6 inhibitors have been the more effective biological agents for treating RA.
IL-17 affects the activity of various cell types that contribute to RA, triggering cartilage bone inflammation and bone destruction. In mouse models, overexpression of IL-17 induces joint inflammation, bone erosion, and cartilage proteoglycan loss. In addition, IL-17 directly inhibits matrix synthesis by chondrocytes and produces enzymes that degrade the cartilage matrix.
TNF-α is commonly expressed in arthropathic tissues and is detected in the synovium of most RA patients. TNF-α stimulates the production of inflammatory mediators such as small molecules like prostaglandins by connective tissue cells and polymorphonuclear cells. Moreover, TNF-α stimulates synoviocytes and chondrocytes, decreases glycoprotein synthesis in osteoclasts, increases glycoprotein degradation, and produces collagenase and other neutral proteases to release osteocalcin, leading to the destruction of bone and cartilage.
Clinical studies have confirmed that the higher the value of VEGF in the peripheral blood of RA patients, the greater the number of involved joints and the more severe the arthropathy. Both IL-1 and TNF-α can promote synovial angiogenesis by up-regulating the secretion of VEGF. Therefore, the level of VEGF in peripheral blood can be used as an evaluation index to reflect the degree of disease in RA patients.
Creative BioMart is a global provider of GMP cytokines and proteins. We are dedicated to providing tailored services for research of glycobiology-related diseases. For inquiries about our products or services, please contact us.
Reference
