作者: Dennis McGonagle , Rik J. U. Lories , Ai Lyn Tan , Michael Benjamin
DOI: 10.1002/ART.22758
关键词:
摘要: The pathogenesis of tissue inflammation and damage in rheumatic diseases that are associated with the major histocompatibility complex (MHC), including rheumatoid arthritis (RA) spondylarthritides (SpA), has mainly been viewed relation to an autoimmune effector mechanism (1–3). However, because synovial joints serve promote movement, it is logical assume aberrant functioning their constituent parts could contribute inflammation. Although such “wear tear” mechanisms well recognized as contributory factors osteoarthritis (OA), less clear intrinsic biomechanical be significant considered autoimmune. Investigators our group previously proposed primary basis for psoriatic (PsA) SpA rather than (4–6). This was based on interpretation magnetic resonance imaging (MRI) knee disease early SpA, which showed specific patterns Moreover, observations were not confined anatomic locations ligaments tendons also affected both magnitude synovitis propensity erosions RA (7). concept tissue-specific or “autoinflammatory factors” (as distinct from autoimmunity, principally played out secondary lymphoid organs) allowed development a new classification scheme all inflammatory disorders (8). Such might underscore common repair pathways may shared by degenerative (9). Thus, purpose present article develop idea joint-specific trigger innate immune responses pivotal players phenotypic expression PsA, related RA, even OA. centered unit we have called synovio-entheseal (SEC) described PsA other types arthropathy.