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10.1111/ajt.13350

http://scihub22266oqcxt.onion/10.1111/ajt.13350
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C5125017!5125017!26079335
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suck abstract from ncbi


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pmid26079335      Am+J+Transplant 2015 ; 15 (9): 2336-45
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  • Hyperlipidemia Promotes Anti-Donor Th17 Responses That Accelerate Allograft Rejection #MMPMID26079335
  • Yuan J; Bagley J; Iacomini J
  • Am J Transplant 2015[Sep]; 15 (9): 2336-45 PMID26079335show ga
  • Hyperlipidemia occurs in 95% of organ transplant recipients, however its effect on organ allograft rejection has not been investigated. We found that induction of hyperlipidemia in mice caused a significant acceleration of rejection of cardiac allografts. Accelerated rejection was associated with an aggressive T cell infiltrate that mediated significant tissue damage as well as increased serum levels of the proinflammatory cytokines IL-2, IL-6, and IL-17. Hyperlipidemic mice had an increased number of Th17 cells in their periphery and rejecting allografts from hyperlipidemic mice contained significant numbers of IL-17 producing T cells that were not detectable in transplants harvested from controls. Neutralization or genetic ablation of IL-17 prolonged survival of cardiac allografts transplanted into hyperlipidemic recipients, suggesting that IL-17 production promotes accelerated rejection. Analysis of alloreactive T cell frequencies directly ex vivo in naïve mice revealed that the frequency of donor reactive IL-17 producing cells in hyperlipidemic was increased prior to antigen exposure, suggesting that hyperlipidemia was sufficient to alter T cell alloreactivity and promote anti-donor Th17 responses on first exposure to antigen. Together, our data suggest that hyperlipidemia alters rejection by altering the types of T cell subsets that respond to donor antigen by promoting Th17 biased anti-donor reactivity.
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