The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Hepatic Ischemia/Reperfusion Injury Involves Functional TLR4 Signaling in Nonparenchymal Cells
Open accessAbstract
Endogenous ligands from damaged cells, so-called damage-associated molecular pattern molecules, can activate innate immunity via TLR4 signaling. Hepatic warm ischemia and reperfusion (I/R) injury and inflammation is largely TLR4 dependent. We produced TLR4 chimeric mice to assess whether the TLR4-dependent injury required TLR4 expression on liver parenchymal or nonparenchymal cells. Chimeric mice were produced by adoptive transfer of donor bone marrow cells into irradiated recipient animals using reciprocal combinations of TLR4 wild-type (WT; C3H/HeOuj) and TLR4 mutant (C3H/HeJ) mouse bone marrow. Wild-type chimeric mice bearing TLR4 mutant hemopoietic cells and TLR4 mutant mice transplanted with their own bone marrow-derived cells were protected from hepatic I/R and exhibited decreased JNK and NF-κB activation compared with WT chimeric mice transplanted with their own bone marrow. In contrast, TLR4 mutant mice transplanted with TLR4 WT bone marrow were not protected from liver I/R and demonstrated pronounced increases in JNK and NF-κB activation when compared with autochthonous transplanted mutant mice. In addition, depletion of phagocytes taking up gadolinium chloride failed to provide any additional protection to TLR4 mutant mice, but substantially reduced damage in WT mice after hepatic I/R. Together, these results demonstrate that TLR4 engagement on actively phagocytic nonparenchymal cells such as Kupffer cells is required for warm I/R-induced injury and inflammation in the liver.
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Reversing established sepsis with antagonists of endogenous high-mobility group box 1
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The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion
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Self-citationHSP70 as Endogenous Stimulus of the Toll/Interleukin-1 Receptor Signal Pathway
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Fibrinogen Stimulates Macrophage Chemokine Secretion Through Toll-Like Receptor 4
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Cited by
TLR4 enhances TGF-β signaling and hepatic fibrosis
Seki, E., De Minicis, S., Österreicher, C. H., Kluwe, J., Osawa, Y., Brenner, D. A., & Schwabe, R. F. (2007) · Nature Medicine · doi:10.1038/nm1663 · Cited by 1,942
HMGB1: Endogenous Danger Signaling
Klune, J. R., Dhupar, R., Cardinal, J., Billiar, T. R., & Tsung, A. (2008) · Molecular Medicine · doi:10.2119/2008-00034.klune · Cited by 762
Self-citationToll‐like receptors and adaptor molecules in liver disease: Update†
Seki, E., & Brenner, D. A. (2008) · Hepatology · doi:10.1002/hep.22306 · Cited by 722
Sterile inflammation in the liver
Kubes, P., & Mehal, W. Z. (2012) · Gastroenterology · doi:10.1053/j.gastro.2012.09.008 · Cited by 666
High‐mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity
Bianchi, M. E., & Manfredi, A. A. (2007) · Immunological Reviews · doi:10.1111/j.1600-065x.2007.00574.x · Cited by 600
Metadata
- Authors
- Tsung, A., Hoffman, R. A., Izuishi, K., Critchlow, N. D., Nakao, A., Chan, M. H., Lotze, M. T., Geller, D. A., & Billiar, T. R.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-12-01
- Volume
- 175
- Issue
- 11
- Pages
- 7661-7668
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2167097725
- Cited by
- 365
- References
- 45
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Tsung, A., Hoffman, R. A., Izuishi, K., Critchlow, N. D., Nakao, A., Chan, M. H., Lotze, M. T., Geller, D. A., & Billiar, T. R. (2005). Hepatic Ischemia/Reperfusion Injury Involves Functional TLR4 Signaling in Nonparenchymal Cells. The Journal of Immunology. https://doi.org/10.4049/jimmunol.175.11.7661
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