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- W2104061060 endingPage "6546" @default.
- W2104061060 startingPage "6536" @default.
- W2104061060 abstract "Preoperative or perioperative ischemic injury of allografts predisposes to graft arteriosclerosis, the major cause of late graft failure. We hypothesize that injured tissues release mediators that increase the production of pathogenic cytokines by alloreactive T cells. We find that freeze-thaw lysates of human endothelial cells (EC) increase both IFN-gamma and IL-17 production by human CD4(+) T cells activated by HLA-DR(+) allogeneic EC. Immunoadsorption of high-mobility group box 1 protein (HMGB1) reduces this activity in the lysates by about one-third, and recombinant HMGB1 increases T cell cytokine production. HMGB1 acts by inducing IL-1beta secretion from contaminating monocytes via TLR4 and CD14. Upon removal of contaminating monocytes, the remaining stimulatory activity of EC lysates is largely attributable to IL-1alpha. Recombinant IL-1 directly augments IFN-gamma and IL-17 production by activated memory CD4(+) T cells, which express IL-1R1. Furthermore, IL-1 increases the frequency of alloreactive memory CD4(+) T cells that produce IL-17, but not those that produce IFN-gamma, in secondary cultures. Our results suggest that IL-1, released by injured EC or by HMGB1-stimulated monocytes, is a key link between injury and enhanced alloimmunity, offering a new therapeutic target for preventing late graft failure." @default.
- W2104061060 created "2016-06-24" @default.
- W2104061060 creator A5022235365 @default.
- W2104061060 creator A5030646863 @default.
- W2104061060 creator A5087363410 @default.
- W2104061060 date "2007-11-15" @default.
- W2104061060 modified "2023-10-17" @default.
- W2104061060 title "IL-1α and IL-1β Are Endogenous Mediators Linking Cell Injury to the Adaptive Alloimmune Response" @default.
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- W2104061060 doi "https://doi.org/10.4049/jimmunol.179.10.6536" @default.
- W2104061060 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17982042" @default.
- W2104061060 hasPublicationYear "2007" @default.
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