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1
Toll-like receptors in systemic autoimmune disease.系统性自身免疫病中的Toll样受体
Nat Rev Immunol. 2006 Nov;6(11):823-35. doi: 10.1038/nri1957.
2
The role of hyaluronan degradation products as innate alloimmune agonists.透明质酸降解产物作为先天性同种免疫激动剂的作用。
Am J Transplant. 2006 Nov;6(11):2622-35. doi: 10.1111/j.1600-6143.2006.01537.x.
3
Interleukin-18 affects local cytokine expression but does not impact on the development of kidney allograft rejection.白细胞介素-18影响局部细胞因子表达，但不影响肾移植排斥反应的发生发展。
Am J Transplant. 2006 Nov;6(11):2612-21. doi: 10.1111/j.1600-6143.2006.01536.x.
4
Expression and regulation of Toll-like receptors in lupus-like immune complex glomerulonephritis of MRL-Fas(lpr) mice.Toll样受体在MRL-Fas(lpr)小鼠狼疮样免疫复合物肾小球肾炎中的表达与调控
Nephrol Dial Transplant. 2006 Nov;21(11):3062-73. doi: 10.1093/ndt/gfl336. Epub 2006 Sep 5.
5
HMGB1 signals through toll-like receptor (TLR) 4 and TLR2.高迁移率族蛋白B1（HMGB1）通过Toll样受体（TLR）4和TLR2发出信号。
Shock. 2006 Aug;26(2):174-9. doi: 10.1097/01.shk.0000225404.51320.82.
6
TLR2 stimulation of intrinsic renal cells in the induction of immune-mediated glomerulonephritis.Toll样受体2刺激肾固有细胞诱导免疫介导性肾小球肾炎。
J Immunol. 2006 Aug 1;177(3):1925-31. doi: 10.4049/jimmunol.177.3.1925.
7
CX3CR1+ interstitial dendritic cells form a contiguous network throughout the entire kidney.CX3CR1+间质树突状细胞在整个肾脏中形成一个连续的网络。
Kidney Int. 2006 Aug;70(3):591-6. doi: 10.1038/sj.ki.5001567. Epub 2006 Jun 7.
8
Toll-like receptor 2 agonists exacerbate accelerated nephrotoxic nephritis.Toll样受体2激动剂会加重加速性肾毒性肾炎。
J Am Soc Nephrol. 2006 Jul;17(7):1931-9. doi: 10.1681/ASN.2005111167. Epub 2006 May 31.
9
New cellular and molecular immune pathways in ischemia/reperfusion injury.缺血/再灌注损伤中的新型细胞与分子免疫途径
Am J Transplant. 2006 Apr;6(4):652-8. doi: 10.1111/j.1600-6143.2005.01228.x.
10
Novel role of toll-like receptor 3 in hepatitis C-associated glomerulonephritis.Toll样受体3在丙型肝炎相关肾小球肾炎中的新作用。
Am J Pathol. 2006 Feb;168(2):370-85. doi: 10.2353/ajpath.2006.050491.

Toll样受体4（TLR4）激活介导肾脏缺血/再灌注损伤。

TLR4 activation mediates kidney ischemia/reperfusion injury.

作者信息

Wu Huiling, Chen Gang, Wyburn Kate R, Yin Jianlin, Bertolino Patrick, Eris Josette M, Alexander Stephen I, Sharland Alexandra F, Chadban Steven J

机构信息

Collaborative Transplant Research Group, Royal Prince Alfred Hospital and Bosch Institute, Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia.

出版信息

J Clin Invest. 2007 Oct;117(10):2847-59. doi: 10.1172/JCI31008.

DOI:10.1172/JCI31008
PMID:17853945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1974864/
Abstract

Ischemia/reperfusion injury (IRI) may activate innate immunity through the engagement of TLRs by endogenous ligands. TLR4 expressed within the kidney is a potential mediator of innate activation and inflammation. Using a mouse model of kidney IRI, we demonstrated a significant increase in TLR4 expression by tubular epithelial cells (TECs) and infiltrating leukocytes within the kidney following ischemia. TLR4 signaling through the MyD88-dependent pathway was required for the full development of kidney IRI, as both TLR4(-/-) and MyD88(-/-) mice were protected against kidney dysfunction, tubular damage, neutrophil and macrophage accumulation, and expression of proinflammatory cytokines and chemokines. In vitro, WT kidney TECs produced proinflammatory cytokines and chemokines and underwent apoptosis after ischemia. These effects were attenuated in TLR4(-/-) and MyD88(-/-) TECs. In addition, we demonstrated upregulation of the endogenous ligands high-mobility group box 1 (HMGB1), hyaluronan, and biglycan, providing circumstantial evidence that one or more of these ligands may be the source of TLR4 activation. To determine the relative contribution of TLR4 expression by parenchymal cells or leukocytes to kidney damage during IRI, we generated chimeric mice. TLR4(-/-) mice engrafted with WT hematopoietic cells had significantly lower serum creatinine and less tubular damage than WT mice reconstituted with TLR4(-/-) BM, suggesting that TLR4 signaling in intrinsic kidney cells plays the dominant role in mediating kidney damage.

摘要

缺血/再灌注损伤（IRI）可能通过内源性配体与Toll样受体（TLR）结合来激活先天性免疫。肾脏中表达的TLR4是先天性激活和炎症的潜在介质。利用肾脏IRI小鼠模型，我们证明了缺血后肾小管上皮细胞（TECs）和肾脏内浸润的白细胞中TLR4表达显著增加。肾脏IRI的充分发展需要通过MyD88依赖途径的TLR4信号传导，因为TLR4（-/-）和MyD88（-/-）小鼠均对肾功能障碍、肾小管损伤、中性粒细胞和巨噬细胞积聚以及促炎细胞因子和趋化因子的表达具有保护作用。在体外，野生型肾脏TECs在缺血后产生促炎细胞因子和趋化因子并发生凋亡。这些作用在TLR4（-/-）和MyD88（-/-）TECs中减弱。此外，我们证明了内源性配体高迁移率族蛋白B1（HMGB1）、透明质酸和双糖链蛋白聚糖的上调，提供了间接证据表明这些配体中的一种或多种可能是TLR4激活的来源。为了确定实质细胞或白细胞中TLR4表达对IRI期间肾脏损伤的相对贡献，我们构建了嵌合小鼠。移植野生型造血细胞的TLR4（-/-）小鼠血清肌酐显著低于用TLR4（-/-）骨髓重建的野生型小鼠，且肾小管损伤较轻，这表明固有肾细胞中的TLR4信号传导在介导肾脏损伤中起主导作用。