Cytokine overproduction, T-cell activation, and defective T-regulatory functions promote nephritis in systemic lupus erythematosus.
Cytokine overproduction, T-cell activation, and defective T-regulatory functions promote nephritis in systemic lupus erythematosus.
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DOI：
10.1155/2010/457146
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发表时间：
2010
影响因子：
--
通讯作者：
Silvestris F
中科院分区：
文献类型：
--
作者：
Tucci M;Stucci S;Strippoli S;Silvestris F
红斑狼疮肾炎（LN）发生在超过三分之一的系统性红斑狼疮患者。其发病机制主要归因于免疫复合物的肾小球沉积和T辅助- (Th-) 1细胞因子的过量产生。在这种情况下，肾小球中IL-12和IL-18的高表达发挥了主要的发病作用。这些细胞因子由巨噬细胞和树突状细胞（dc）在局部产生，它们吸引其他炎症细胞，导致肾脏炎症的维持。然而，包括t细胞和b细胞在内的其他细胞群在肾损害的发展和恶化中是不可或缺的。t细胞包括许多致病亚群，与t调节（Treg）细胞功能缺陷保持一致的Th-17的激活被认为是导致肾小球损伤的进一步事件。这些群体也激活b细胞产生肾源性自身抗体。因此，LN包括一个复杂的发病机制，涉及不同的参与者，评估他们的活动可能为监测疾病的发病提供有效的工具。
Lupus nephritis (LN) occurs in more than one-third of patients with systemic lupus erythematosus. Its pathogenesis is mostly attributable to the glomerular deposition of immune complexes and overproduction of T helper- (Th-) 1 cytokines. In this context, the high glomerular expression of IL-12 and IL-18 exerts a major pathogenetic role. These cytokines are locally produced by both macrophages and dendritic cells (DCs) which attract other inflammatory cells leading to maintenance of the kidney inflammation. However, other populations including T-cells and B-cells are integral for the development and worsening of renal damage. T-cells include many pathogenetic subsets, and the activation of Th-17 in keeping with defective T-regulatory (Treg) cell function regards as further event contributing to the glomerular damage. These populations also activate B-cells to produce nephritogenic auto-antibodies. Thus, LN includes a complex pathogenetic mechanism that involves different players and the evaluation of their activity may provide an effective tool for monitoring the onset of the disease.
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