|Description||Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the "shared epitope" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA.|
Hydroxychloroquine sulfate [DR:D02114]
Certolizumab pegol [DR:D03441]
|Other DBs||ICD-10: M05
|Reference||PMID:27338350 (gene, drug)
Chung IM, Ketharnathan S, Thiruvengadam M, Rajakumar G
Rheumatoid Arthritis: The Stride from Research to Clinical Practice.
Int J Mol Sci 17:E900 (2016)
Papadakis MA and McPhee SJ |(ed)
Current Medical Diagnosis & Treatment 2015, Fifty-Fourth Edition
McGraw Hill Education
Meier FM, Frerix M, Hermann W, Muller-Ladner U
Current immunotherapy in rheumatoid arthritis.
Immunotherapy 5:955-74 (2013)
Boissier MC, Semerano L, Challal S, Saidenberg-Kermanac'h N, Falgarone G
Rheumatoid arthritis: from autoimmunity to synovitis and joint destruction.
J Autoimmun 39:222-8 (2012)