title: Pathways of cell activation in spondyloarthropathies.
abstract: The initiating event in cell activation is unknown in most autoimmune diseases. The role of infection is clear in some cases, especially in reactive arthritis; however, there is little evidence of a specific organism in other spondyloarthropathies. Common pathways of cell-cell interaction and activation manifest in inflammation, but subtle differences may exist. The presence of T cells, macrophages, and B-lymphocytes suggest an autoimmune mechanism; the arthritogenic peptide theory has been proposed. Furthermore, the association of spondyloarthropathies with HLA-B27 suggests it may be important in synovial T-cell activation. Other cell types involved in the process of bone and cartilage destruction, including fibroblasts and osteoclasts, may also be activated. Endothelial activation and angiogenesis may be a critical primary event in these diseases. Finally, trauma (physical or psychological) in the form of stress may be an important factor; the nervous system and neuropeptides may play a role in cell activation and initiation of arthritis.
authors.affiliation: The Department of Rheumatology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.
authors.forename: U
authors.initials: U
authors.lastname: Fearon
authors.forename: D J
authors.initials: DJ
authors.lastname: Veale
mesh_terms: D002455:Cell Division / Q000502:physiology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology*; D006801:Humans; D008264:Macrophages / Q000502:physiology*; D009389:Neovascularization, Pathologic; D010011:Osteocytes / Q000502:physiology*; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D013131:Spine / Q000098:blood supply*; D025242:Spondylarthropathies / Q000209:etiology / Q000503:physiopathology*