A. González-Cortés, S. Guerrero, E. Sánchez-Tirado, M.L. Agüí, P. Yáñez-Sedeño, J.M. Pingarrón
Rheumatoid arthritis is an autoimmune disorder characterized by persistent erosive synovitis, systemic inflammation and the presence of autoantibodies, particularly rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCPA) antibodies, which play an important role in inducing inflammation and joint damage, releasing pro-inflammatory cytokines from monocytes and macrophages [1,2]. Likewise, neutrophil activating protein-2 (CXCL7) is a platelet-derived growth factor belonging to the CXC chemokine subfamily, which is expressed in serum, synovial fluid and synovial tissue of patients developing rheumatoid arthritis during the first twelve weeks, being useful to reflect local pathological changes [3]. Besides, matrix metalloproteinase-3 (MMP-3), which is induced by inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α) in rheumatoid synovium, degrades several extracellular matrix components of cartilage and plays central roles in rheumatoid joint destruction [4]. Thereby, monitoring serum RF, CCPA, CXCL7 and MMP-3 levels is useful for predicting the disease activity in rheumatoid arthritis.