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Review
. 2010 Apr;6(4):224-35.
doi: 10.1038/nrneph.2010.16. Epub 2010 Feb 23.

The role of Toll-like receptors in renal diseases

Affiliations
Review

The role of Toll-like receptors in renal diseases

Anna Gluba et al. Nat Rev Nephrol. 2010 Apr.

Abstract

Toll-like receptors (TLRs) have a key role in innate immunity. These receptors recognize both pathogen-associated molecular patterns and molecules that are released from damaged tissue. TLRs mediate signal transduction pathways through the activation of transcription factors that regulate the expression of proinflammatory cytokines and chemokines and are required for the development of adaptive immune responses. TLRs might have an important role in the pathogenesis of renal diseases: their exaggerated activation is associated with ischemic kidney damage, acute kidney injury, end-stage renal failure, acute tubulointerstitial nephritis, acute renal transplant rejection and delayed allograft function. As the results of previous studies concerning the role of TLRs in renal diseases are conflicting, further work is needed to determine the exact role of these receptors and to evaluate strategies to prevent TLR-mediated local inflammation. This Review discusses the evidence supporting a role for TLRs in contrasting bacterial infections and in causing or aggravating renal conditions when TLR activation leads to a harmful inflammatory response.

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References

    1. Am J Pathol. 2006 Feb;168(2):370-85 - PubMed
    1. Cell Host Microbe. 2007 Jun 14;1(4):287-98 - PubMed
    1. Science. 2004 Mar 5;303(5663):1522-6 - PubMed
    1. Clin Infect Dis. 1995 Jul;21(1):1-6; quiz 7-8 - PubMed
    1. J Am Soc Nephrol. 2006 Dec;17(12):3365-73 - PubMed

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