The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Adenosine A2A receptor activation reduces hepatic ischemia reperfusion injury by inhibiting CD1d-dependent NKT cell activation
Open accessAbstract
Ischemia reperfusion injury results from tissue damage during ischemia and ongoing inflammation and injury during reperfusion. Liver reperfusion injury is reduced by lymphocyte depletion or activation of adenosine A2A receptors (A2ARs) with the selective agonist 4- {3-[6-amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]- prop-2-ynyl}-cyclohexanecarboxylic acid methyl ester (ATL146e). We show that NKT cells are stimulated to produce interferon (IFN)-γ by 2 h after the initiation of reperfusion, and the use of antibodies to deplete NK1.1-positive cells (NK and NKT) or to block CD1d-mediated glycolipid presentation to NKT cells replicates, but is not additive to, the protection afforded by ATL146e, as assessed by serum alanine aminotransferase elevation, histological necrosis, neutrophil accumulation, and serum IFN-γ elevation. Reduced reperfusion injury observed in RAG-1 knockout (KO) mice is restored to the wild-type (WT) level by adoptive transfer of NKT cells purified from WT or A2AR KO mice but not IFN-γ KO mice. Additionally, animals with transferred A2AR−/− NKT cells are not protected from hepatic reperfusion injury by ATL146e. In vitro, ATL146e potently inhibits both anti-CD3 and α-galactosylceramide–triggered production of IFN-γ by NKT cells. These findings suggest that hepatic reperfusion injury is initiated by the CD1d-dependent activation of NKT cells, and the activation of these cells is inhibited by A2AR activation.
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Lysosomal Glycosphingolipid Recognition by NKT Cells
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Cited by
Invariant natural killer T cells: an innate activation scheme linked to diverse effector functions
Brennan, P. J., Brigl, M., & Brenner, M. B. (2013) · Nature Reviews Immunology · doi:10.1038/nri3369 · Cited by 835
Purinergic regulation of the immune system
Cekic, C., & Linden, J. (2016) · Nature Reviews Immunology · doi:10.1038/nri.2016.4 · Cited by 787
Self-citationAdenosine, an endogenous distress signal, modulates tissue damage and repair
Fredholm, B. B. (2007) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4402132 · Cited by 686
Hypoxia signaling in human diseases and therapeutic targets
Lee, J. W., Ko, J., Ju, C., & Eltzschig, H. K. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0235-1 · Cited by 384
Tissue-specific functions of invariant natural killer T cells
Crosby, C. M., & Kronenberg, M. (2018) · Nature Reviews Immunology · doi:10.1038/s41577-018-0034-2 · Cited by 367
Metadata
- Authors
- Lappas, C. M., Day, Y.-J., Marshall, M. A., Engelhard, V. H., & Linden, J.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-11-06
- Volume
- 203
- Issue
- 12
- Pages
- 2639-2648
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2097354544
- Cited by
- 295
- References
- 42
- FWCI
- 11.67
- Type
- journal article
- Language
- en
- Open access
- green
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- Lappas, C. M., Day, Y.-J., Marshall, M. A., Engelhard, V. H., & Linden, J. (2006). Adenosine A2A receptor activation reduces hepatic ischemia reperfusion injury by inhibiting CD1d-dependent NKT cell activation. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20061097
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