Journal
CLINICAL IMMUNOLOGY
Volume 130, Issue 1, Pages 41-50Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2008.08.016
Keywords
Ischemia reperfusion injury; Innate immunity; Inflammation
Categories
Funding
- US National Institutes of Health
- US National Kidney Foundation
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK054770] Funding Source: NIH RePORTER
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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. (c) 2008 Elsevier Inc. All rights reserved.
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