The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
TLR2 Is Constitutively Expressed within the Kidney and Participates in Ischemic Renal Injury through Both MyD88-Dependent and -Independent Pathways
Abstract
TLRs are an evolutionarily conserved family of cell membrane proteins believed to play a significant role in innate immunity and the response to tissue injury, including that induced by ischemia. TLR signaling pathways activate transcription factors that regulate expression of prosurvival proteins, as well as proinflammatory cytokines and chemokines through one of two proximal adapter proteins, MyD88 or Toll/IL-1R domain-containing adaptor-inducing IFN-β (Trif). Our study defines the constitutive protein expression of TLR2 in kidneys of humans and mice, and provides insight into the signaling mechanisms by which a deficiency of TLR2 protects from ischemic organ injury. Our study compared and contrasted the effects of renal ischemia in wild-type mice and mice deficient in TLR2, MyD88, Trif, and MyD88 × Trif. TLR2 protein was evident in many cell types in the kidney, including renal tubules of the outer stripe of the medulla, glomeruli, and in the renal vasculature. The pattern of protein expression was similar in humans and mice. The absence of TLR2, MyD88, and MyD88 × Trif conferred both physiologic and histologic protection against sublethal ischemia at 24 h. Interestingly, TLR2-deficient mice were better protected from ischemic renal injury than those deficient for the adapter protein MyD88, raising the intriguing possibility that TLR-2-dependent/MyD88-independent pathways also contribute to kidney injury. We conclude that TLR2 protein is constitutively expressed in the kidney and plays an important role in the pathogenesis of acute ischemic injury by signaling both MyD88-dependent and MyD88-independent pathways.
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Cytokine Serum Level During Severe Sepsis in Human IL-6 as a Marker of Severity
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Self-citationTLR Signaling in the Gut in Health and Disease
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Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney
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Extracellular Histones Are Mediators of Death through TLR2 and TLR4 in Mouse Fatal Liver Injury
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Inflammation in Acute Kidney Injury
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Toll-Like Receptor 4 Promotes Tubular Inflammation in Diabetic Nephropathy
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McSweeney, K. R., Gadanec, L. K., Qaradakhi, T., Ali, B. A., Zulli, A., & Apostolopoulos, V. (2021) · Cancers · doi:10.3390/cancers13071572 · Cited by 363
Metadata
- Authors
- Shigeoka, A. A., Holscher, T. D., King, A. J., Hall, F. W., Kiosses, W. B., Tobias, P. S., Mackman, N., & McKay, D. B.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-05
- Volume
- 178
- Issue
- 10
- Pages
- 6252-6258
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1940749453
- Cited by
- 273
- References
- 43
- FWCI
- 15.00
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: TLR2 Is Constitutively Expressed within the Kidney and Participates in Ischemic Renal Injury through Both MyD88-Dependent and -Independent Pathways. https://app.cochat.ai/papers/10.4049/jimmunol.178.10.6252
- The paper
- Shigeoka, A. A., Holscher, T. D., King, A. J., Hall, F. W., Kiosses, W. B., Tobias, P. S., Mackman, N., & McKay, D. B. (2007). TLR2 Is Constitutively Expressed within the Kidney and Participates in Ischemic Renal Injury through Both MyD88-Dependent and -Independent Pathways. The Journal of Immunology. https://doi.org/10.4049/jimmunol.178.10.6252
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