The Pathogenesis and Therapeutic Implications of Tubulointerstitial Inflammation in Human Lupus Nephritis.
The Pathogenesis and Therapeutic Implications of Tubulointerstitial Inflammation in Human Lupus Nephritis.
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DOI：
10.1016/j.semnephrol.2015.08.007
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发表时间：
2015-09
影响因子：
3.3
通讯作者：
Chang A
中科院分区：
文献类型：
--
作者：
Clark MR;Trotter K;Chang A
肾炎是系统性红斑狼疮（SLE）的常见并发症，目前的治疗往往证明是不够的。目前的狼疮肾炎分类系统强调肾小球的敏锐度和瘢痕形成。然而，肾小管间质炎症（TII）和瘢痕形成是进展为肾衰竭的更好的预测因子。现在越来越清楚的是，免疫学特征和可能的潜在机制，是非常不同的狼疮性肾小球肾炎（GN）和TII在活检时。虽然GN是系统性自身免疫的表现，但TII与局部原位适应性免疫细胞网络相关，预测其会放大局部炎症和组织损伤。此外，先天免疫细胞和效应物的网络定义不清可能导致局部炎症的严重程度。了解这些原位免疫机制将有助于更好地了解狼疮性肾炎的临床意义，并揭示新的治疗机会。
Nephritis is a common complication of systemic lupus erythematosus (SLE) for which current therapies often prove inadequate. Current lupus nephritis classification systems emphasize glomerular acuity and scarring. However, tubulointerstitial inflammation (TII) and scarring are much better predictors of progression to renal failure. It is now becoming clear that the immunological features, and probable underlying mechanisms, are very different in lupus glomerulonephritis (GN) and TII at time of biopsy. While GN is a manifestation of systemic autoimmunity, TII is associated with local, in situ adaptive immune cell networks predicted to amplify local inflammation and tissue damage. In addition, poorly defined networks of innate immune cells and effectors likely contribute to the severity of local inflammation. Understanding these in situ immune mechanisms should lead to a better understanding of prognostically meaningful lupus nephritis subsets and reveal novel therapeutic opportunities.