The role of cytokines, chemokines, and adhesion molecules in the pathogenesis of idiopathic inflammatory myopathies.
The role of cytokines, chemokines, and adhesion molecules in the pathogenesis of idiopathic inflammatory myopathies.
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DOI：
10.1007/s11926-000-0082-y
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发表时间：
2000-06-01
影响因子：
5
通讯作者：
Lundberg, I E
中科院分区：
文献类型：
--
作者：
Lundberg, I E
细胞因子、趋化因子和粘附分子是慢性炎症和免疫调节中的重要介质。在特发性炎性肌病（IIM）中，在肌肉中观察到促炎细胞因子（特别是白细胞介素（IL）-1 α和IL-1 β、肿瘤坏死因子（TNF）-α和巨噬细胞炎性蛋白（MIP）-1 α）以及抑制性细胞因子转化生长因子（TGF）-β的表达增加。在多发性肌炎、皮肌炎和包涵体肌炎之间，细胞因子和趋化因子模式没有差异，这可能表明在这些肌炎亚型中涉及相似的发病机制。在活动性炎症患者和无炎症的慢性持续性肌无力患者中，内皮细胞中IL-1 α表达的突出发现使其成为理解肌无力发病机制的有趣分子。参与肌炎的发病机制的血管进一步支持的粘附分子的表达增加和内皮细胞的表型表达，类似于高内皮小静脉在所有三个子集的IIM。迄今为止的分子研究表明，微血管在IIM的发病机制中的作用不仅在DM中，如先前所建议的，而且在PM和IBM中。这些研究还表明，IL-1 α可能是新的治疗干预的靶分子。
Cytokines, chemokines, and adhesion molecules are important mediators in chronic inflammation and in immune regulation. In idiopathic inflammatory myopathies (IIM), increased expression of proinflammatory cytokines particularly interleukin (IL)-1alpha and IL-1beta, tumor necrosis factor (TNF)-alpha and macrophage inflammatory proteins (MIP)-1alpha, as well as of the inhibitory cytokines transforming growth factor (TGF)-beta was observed in muscle. There was no difference in cytokine and chemokine pattern between polymyositis, dermatomyositis, and inclusion body myositis, which could indicate that similar pathogenetic mechanisms are involved in these subsets of myositis. A prominent finding of IL-1alpha expression in endothelial cells, both in patients with active inflammation and in patients with chronic persisting muscle weakness without inflammation, makes this an interesting molecule in understanding the mechanisms for the pathogenesis of muscle weakness. Involvement of the blood vessels in the pathogenesis of myositis was further supported by increased expression of adhesion molecules and by a phenotypical expression of endothelial cells, resembling high endothelium venules in all three subsets of IIM. The molecular studies to date indicate a role of the microvessels in the pathogenesis of IIM not only in DM, as was previously suggested, but also in PM and IBM. The studies also indicate that IL-1alpha could be a target molecule for new therapeutical interventions.