Rheumatoid arthritis

Abstract

Rheumatoid arthritis is a systemic, inflammatory, autoimmune disorder. Enhanced understanding of molecular pathogenesis has enabled development of innovative biological agents that target specific parts of the immune system. These treatments have changed the course and face of rheumatoid arthritis and outcomes for patients and society. New knowledge has emerged of how environmental factors interact with susceptibility genes and the immune system in the pathogenesis of a major subset of rheumatoid arthritis. Research undertaken on the longitudinal disease process and molecular pathology of joint inflammation has led to new therapeutic strategies that promote early use of disease-modifying drugs with tight disease control and distinct and quantifiable treatment goals. Today, such approaches can halt most cases of joint destruction but not all instances of joint inflammation and comorbidity. Understanding the cause and pathogenesis of different rheumatoid arthritis subsets will lead not only to individualised treatments during early phases of the illness but also, possibly, to disease prevention.

Bone Morphogenetic Protein 2 and Transforming Growth Factor β1 Inhibit the Expression of the Proinflammatory Cytokine IL-34 in Rheumatoid Arthritis Synovial Fibroblasts

“…1 Among the cells located in the inflamed joint, synovial fibroblasts are crucial players driving inflammation and bone erosion. 2 IL-34, 3 basically described as promoting monocyte proliferation and survival, and osteoclast differentiation, 4 is expressed by synovial fibroblasts of RA patients.…”

Secondary Osteoarthritis in Rheumatoid Arthritis

“…РА поражает приблизительно 1 % населения [5] и характеризуется воспалением суставов, которое мо-жет привести к суставной деструкции и системным осложнениям [6].…”

HLA-DPB1-COL11A2 and three additional xMHC loci are independently associated with RA in a UK cohort

“…It is an inflammatory, autoimmune, systemic disease and is characterized by the chronic inflammation and progressive destruction of the joints that leads to disability. 1 RA is a complex disease, meaning that multiple genetic variants, environmental factors and random events interact to trigger pathological pathways. Although many of these etiological factors have not yet been identified, recent groundbreaking advances such as the availability of genome-wide association studies have expanded our knowledge about the genetic factors that contribute to RA, such that 26 loci have now been confirmed (Po5 Â 10 À8 ).…”