肾脏在缺血-再灌注损伤后不久就开始修复，此时肾组织中单核-巨噬细胞系统( MoPh )发生表型转化，参与了抑制炎症和促进修复的过程；而IKKα-p52:RelB途径在抑制炎症反应和促进细胞增殖过程中起重要的作用。我们的前期研究表明，肾脏IR损伤后修复时， M2型MoPh和Treg 浸润明显，间质中IL-10、CXCL12和肾小管上皮细胞内IKKα表达升高。但MoPh内IKKα是否活化？是否通过IKKα-p52:RelB途径活化参与修复的？尚不清楚。我们假设：MoPh内IKKα-p52:RelB途径被激活后，一方面介导Treg成熟并释放IL-10；另一方面，启动并维持CXCL12的表达，最终促进细胞迁移，增殖，修补丢失的肾小管上皮细胞，恢复肾脏功能。本研究使用基因敲除小鼠，采用体外细胞共培养，体内细胞过继转移等技术，阐明Mpoh参与肾脏修复的机制，为探索急性肾损伤治疗的新靶点提供理论依据。

The recovery and regeneration usually occurs shortly (between 24 and 72 hours) post-ischemia, during which cellular dedifferentiation and tubular epithelial cell proliferation occur. There is compelling evidence that the renal mononuclear phagocytic system (Moph) actively participates in the resolution of injury and promotes tissue restoration in the phase after renal ischemia reperfusion (IR) injury. Several lines of evidence suggest that the IKKα-driven noncanonical NFκB p52:RelB signaling pathway is critical in the regression of acute inflammation and the process of keratinocyte and endothelium proliferation and differentiation. Our previous studies revealed that IKKα activation in tubular epithelial cells mediated kidney self repair by infiltrating T regular cells, promoting anti-inflammatory cytokine IL-10, chemotactic factor CXCL12 ( also be named as stromal cell-derived factor 1, SDF-1) synthesis. To further investigate whether KKα-driven noncanonical NFκB p52:RelB signaling pathway is activated in Moph in the repair phase. We hypothesized that activation of this signaling pathway in Moph would participate in the survived tubular epithelial cells proliferation and kidney repair after renal IR injury by two possible ways: 1. to mediate Treg cells developing, maturation and releasing IL-10 ; 2. to initiate and sustain the expression of CXCL12, which result in the survived tubular epithelial cells migration, dedifferentiation, proliferation and repairs the injured tubular cells. To test this hypothesis, monocytes, na?ve T cells and tubular epithelial cells will be isolated and co-cultured in vitro and Moph adoptive transfer will be used in vivo in this study, in order to elucidate the molecular mechanism of IKKα-driven noncanonical NFκB p52:RelB signaling pathway in Moph in promoting tubular epithelial cell regeneration and kidney repair , and further to provide a novel clue for preventing and treating ischemic acute kidney injury.