Fearon U, Veale D J
The Department of Rheumatology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.
Curr Rheumatol Rep. 2001 Oct;3(5):435-42. doi: 10.1007/s11926-996-0015-5.
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.
在大多数自身免疫性疾病中，细胞激活的起始事件尚不清楚。在某些情况下，感染的作用是明确的，尤其是在反应性关节炎中；然而，在其他脊柱关节病中，几乎没有证据表明存在特定的病原体。细胞间相互作用和激活的常见途径表现为炎症，但可能存在细微差异。T细胞、巨噬细胞和B淋巴细胞的存在提示自身免疫机制；有人提出了致关节炎肽理论。此外，脊柱关节病与HLA - B27的关联表明，它可能在滑膜T细胞激活中起重要作用。参与骨和软骨破坏过程的其他细胞类型，包括成纤维细胞和破骨细胞，也可能被激活。内皮细胞激活和血管生成可能是这些疾病中的一个关键原发性事件。最后，压力形式的创伤（身体或心理）可能是一个重要因素；神经系统和神经肽可能在细胞激活和关节炎的起始中起作用。
