Kinsey Gilbert R, Li Li, Okusa Mark D
Division of Nephrology and Center for Immunity, Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA.
Nephron Exp Nephrol. 2008;109(4):e102-7. doi: 10.1159/000142934. Epub 2008 Sep 18.
Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI) and evidence supporting the involvement of both innate and adaptive immunity in renal IRI has accumulated in recent years. In addition to leukocytes, kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability. Kidney tubular epithelial cells increase complement binding and upregulate toll-like receptors, both of which lead to cytokine/chemokine production in IRI. Activation of kidney resident dendritic cells, interferon-gamma-producing neutrophils, infiltrating macrophages, CD4+ T cells, B cells and invariant natural killer T cells are all implicated in the pathogenesis of AKI. The complex interplay between innate and adaptive immunity in renal IRI is still not completely understood, but major advances have been made. This review summarizes these recent advances to further our understanding of the immune mechanisms of acute kidney injury.
缺血再灌注损伤（IRI）是急性肾损伤（AKI）的主要原因之一，近年来，支持先天性免疫和适应性免疫参与肾脏IRI的证据不断积累。除白细胞外，肾内皮细胞通过增加黏附分子表达和血管通透性，在IRI后促进炎症反应。肾小管上皮细胞增加补体结合并上调Toll样受体，这两者都会导致IRI中细胞因子/趋化因子的产生。肾脏驻留树突状细胞、产生干扰素-γ的中性粒细胞、浸润的巨噬细胞、CD4+T细胞、B细胞和不变自然杀伤T细胞的激活均与AKI的发病机制有关。肾脏IRI中先天性免疫和适应性免疫之间复杂的相互作用仍未完全了解，但已取得了重大进展。本综述总结了这些最新进展，以加深我们对急性肾损伤免疫机制的理解。
