McGuire M K, Meats J E, Ebsworth N M, Murphy G, Reynolds J J, Russell R G
Int J Immunopharmacol. 1982;4(2):91-102. doi: 10.1016/0192-0561(82)90056-x.
Destruction of joint structures in arthritis may result from failure of normal mechanisms controlling interactions among cells of the various tissues of the joint. Normal synovium in culture produces less prostaglandin E (PGE) and collagenase than rheumatoid. When rheumatoid synovium is dissociated into cells, the adherent cell cultures rapidly lose the ability to synthesize large amounts of PGE and collagenase and become indistinguishable from normal synovial cells. A mononuclear cell factor (MCF) derived from supernatant media of cultured human blood mononuclear cells and a 'synovial factor(s)' (SF) from cultures of either normal or rheumatoid synovial fragments both stimulate production of PGE and proteinase by cells derived from human synovium, cartilage and bone. The activities of factors which may be present in these stimulatory supernatants may be unmasked in vitro when they are removed from the normal control present in vivo. Normal synovium probably contains cells which, with the appropriate stimulus, may be recruited to participate in joint tissue degradation. Normal connective tissue turnover may also be controlled by a neutral metallo-proteinase inhibitor (TIMP), which is produced in considerable amounts by normal synovium, but which cannot be detected in cultures of rheumatoid synovium. While corticosteroids inhibit the production and action of MCF and SF, they stimulate production of TIMP by normal or rheumatoid synovial tissue in vitro and may contribute to the endogenous control mechanisms. PGE may also have a modulatory role in these cellular interactions.
关节炎中关节结构的破坏可能源于控制关节各组织细胞间相互作用的正常机制失效。培养的正常滑膜产生的前列腺素E（PGE）和胶原酶比类风湿滑膜少。当类风湿滑膜解离成细胞时，贴壁细胞培养物迅速失去合成大量PGE和胶原酶的能力，变得与正常滑膜细胞难以区分。源自培养的人血单核细胞上清培养基的单核细胞因子（MCF）和来自正常或类风湿滑膜碎片培养物的“滑膜因子”（SF）均刺激源自人滑膜、软骨和骨的细胞产生PGE和蛋白酶。当这些刺激性上清液中可能存在的因子从体内存在的正常控制中移除时，其活性可能在体外被揭示。正常滑膜可能含有在适当刺激下可被募集参与关节组织降解的细胞。正常结缔组织的更新也可能受中性金属蛋白酶抑制剂（TIMP）控制，正常滑膜大量产生TIMP，但在类风湿滑膜培养物中无法检测到。虽然皮质类固醇抑制MCF和SF的产生及作用，但它们在体外刺激正常或类风湿滑膜组织产生TIMP，可能有助于内源性控制机制。PGE在这些细胞相互作用中也可能具有调节作用。
