Epstein–Barr virus and rheumatoid arthritis is there a link.docVIP

Available online /content/8/1/204 Review Epstein–Barr virus and rheumatoid arthritis: is there a link? Karen H Costenbader and Elizabeth W Karlson Brigham and Women’s Hospital, Division of Rheumatology, Immunology and Allergy, Department of Medicine, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA Corresponding author: Karen H Costenbader, kcostenbader@ Published: 16 January 2006 Arthritis Research Therapy 2006, 8:204 (doi:10.1186/ar1893) This article is online at /content/8/1/204 ? 2006 BioMed Central Ltd Abstract inflammatory cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α), as well as proteolytic enzymes, destroying synovium, cartilage, and underlying bone [11]. The T cells infiltrating the rheumatoid synovium are oligoclonal, implicating an antigen-driven process [12,13], but the inciting antigen or antigens remain unidentified. Activated T cells also signal B cells to produce increased levels of immunoglobulins, including rheumatoid factor (RF). Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic, destructive, debilitating arthritis. Its etiology is unknown; it is presumed that environmental factors trigger development in the genetically predisposed. Epstein–Barr virus, a nearly ubiquitous virus in the human population, has generated great interest as a potential trigger. This virus stimulates polyclonal lymphocyte expansion and persists within B lymphocytes for the host’s life, inhibited from reactivating by the immune response. In latent and replicating forms, it has immunomodulating actions that could play a role in the development of this autoimmune disease. The evidence linking Epstein–Barr virus and rheumatoid arthritis is reviewed. Autoreactive B cells also have a central role in the development of RA, producing autoantibodies that might be involved i