B Cells Limit Repair after Ischemic Acute Kidney Injury

Jang, Hye Ryoun; Gandolfo, Maria Teresa; Ko, Gang Jee; Satpute, Shailesh R.; Racusen, Lorraine C.; Rabb, Hamid

doi:10.1681/asn.2009020182

Cited by 92 publications

(74 citation statements)

References 51 publications

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“…IL-10 has been implicated in ameliorating renal tissue injury under different pathophysiologic conditions. 27 Consistent with these reports, our results show that the ability of DN T cells to improve the course of ischemia-mediated AKI was IL-10 dependent. Thus, while kidney DN T cells can suppress CD4 T cell proliferation, peripheral gld DN T cells can suppress IRIinduced AKI.…”

Section: Epithelia Our Previous Results Show That Cd4supporting

confidence: 92%

Double-Negative αβ T Cells Are Early Responders to AKI and Are Found in Human Kidney

Martina¹,

Noel²,

Saxena³

et al. 2016

Journal of the American Society of Nephrology

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Section: Epithelia Our Previous Results Show That Cd4supporting

confidence: 92%

Double-Negative αβ T Cells Are Early Responders to AKI and Are Found in Human Kidney

Martina¹,

Noel²,

Saxena³

et al. 2016

Journal of the American Society of Nephrology

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“…We found a significant decrease of the antiapoptotic Bcl-2 after renal ischemia/reperfusion, reversed by PACAP treatment [15]. Cytokines and chemokines also play an important role in the development of kidney injury after ischemia/reperfusion [6,18,19,49]. PACAP decreased proinflammatory cytokines, like TNF-α and IL-6, in different pathological conditions in the kidney [27].…”

Section: Effect Of Exogenous Pacap In Ischemia/reperfusion-induced Kimentioning

confidence: 65%

The effects of pituitary adenylate cyclase activating polypeptide in renal ischemia/reperfusion

László¹,

Kiss²,

Horváth³

et al. 2014

Acta Biologica Hungarica

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pituitary adenylate cyclase activating polypeptide (pacap) is a multifunctional neuropeptide occurring in the nervous system as well as in the peripheral organs. Beneficial action of PACAP has been shown in different pathological processes. The strong protective effects of the peptide are probably due to its complex modulatory actions in antiapoptotic, anti-inflammatory and antioxidant pathways. In the kidney, PACAP is protective in models of diabetic nephropathy, myeloma kidney injury, cisplatin-, gentamycinand cyclosporin-induced damages. Numerous studies have been published describing the protective effect of this peptide in renal ischemia/reperfusion. the present review focuses on the ischemia/reperfusioninduced kidney injury and gives a brief summary about the results published in this area.

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“…Blockade of TLR2, however, has recently been tested in humans and is in phase 2 trials in the United States and Europe (OPN-305; Opsona Therapeutics). 31 Virtually all immune cells have been implicated in AKI, and some are thought to be deleterious (e.g., neutrophils, 10,16 monocytes/macrophages, 25,32 DCs, 33,34 NKT cells, 17,35 NK cells, 19 and B cells 18,36 ), whereas others are likely protective (e.g., Tregs 20,21 ). Others, such as macrophages, play different roles depending on the type and time at which they arrive in the injured tissue.…”

Section: Basic Concepts Of Inflammationmentioning

confidence: 99%

Inflammation in AKI

Rabb

Griffin

McKay

et al. 2016

Journal of the American Society of Nephrology

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343

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Inflammation is a complex biologic response that is essential for eliminating microbial pathogens and repairing tissue after injury. AKI associates with intrarenal and systemic inflammation; thus, improved understanding of the cellular and molecular mechanisms underlying the inflammatory response has high potential for identifying effective therapies to prevent or ameliorate AKI. In the past decade, much knowledge has been generated about the fundamental mechanisms of inflammation. Experimental work in small animal models has revealed many details of the inflammatory response that occurs within the kidney after typical causes of AKI, including insights into the molecular signals released by dying cells, the role of pattern recognition receptors, the diverse subtypes of resident and recruited immune cells, and the phased transition from destructive to reparative inflammation. Although this expansion of the basic knowledge base has increased the number of mechanistically relevant targets of intervention, progress in developing therapies that improve AKI outcomes by modulation of inflammation remains slow. In this article, we summarize the most important recent developments in understanding the inflammatory mechanisms of AKI, highlight key limitations of the commonly used animal models and clinical trial designs that may prevent successful clinical application, and suggest priority approaches for research toward clinical translation in this area.

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B Cells Limit Repair after Ischemic Acute Kidney Injury

Abstract: There is no established modality to repair kidney damage resulting from ischemia-reperfusion injury (IRI). Early responses to IRI involve lymphocytes, but the role of B cells in tissue repair after IRI is unknown.

Cited by 92 publications

References 51 publications

Double-Negative αβ T Cells Are Early Responders to AKI and Are Found in Human Kidney

Double-Negative αβ T Cells Are Early Responders to AKI and Are Found in Human Kidney

The effects of pituitary adenylate cyclase activating polypeptide in renal ischemia/reperfusion

Inflammation in AKI

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