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Clin Immunol. 2009 Jan;130(1):41-50. doi: 10.1016/j.clim.2008.08.016. Epub 2008 Oct 14.

The innate immune response in ischemic acute kidney injury.

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1
Nephrology Division, Department of Medicine, Johns Hopkins University School of Medicine, Ross Building, Room 965, 720 Rutland Avenue, Baltimore, MD 21205, USA.

Abstract

Kidney ischemia reperfusion injury is a major cause of morbidity in both allograft and native kidneys. Ischemia reperfusion-induced acute kidney injury is characterized by early, alloantigen-independent inflammation. Major components of the innate immune system are activated and participate in the pathogenesis of acute kidney injury, plus prime the allograft kidney for rejection. Soluble members of innate immunity implicated in acute kidney injury include the complement system, cytokines, and chemokines. Toll-like receptors (TLRs) are also important contributors. Effector cells that participate in acute kidney injury include the classic innate immune cells, neutrophils and macrophages. Recent data has unexpectedly identified lymphocytes as participants of early acute kidney injury responses. In this review, we will focus on immune mediators that participate in the pathogenesis of ischemic acute kidney injury.

PMID:
18922742
PMCID:
PMC2646108
DOI:
10.1016/j.clim.2008.08.016
[Indexed for MEDLINE]
Free PMC Article
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