2009
DOI: 10.1016/j.healun.2008.06.012
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Interleukin-6 Deficiency Fails to Prevent Chronic Rejection After Aortic Allografts in Apolipoprotein E–Deficient Mice

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Cited by 6 publications
(4 citation statements)
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“…7 Chronic rejection models have been used widely to investigate the pathogenesis of chronic vascular rejection. [8][9][10][11][12][13] In conclusion, size discrepancy between donor and recipient aortas is not in obstacle in a mouse heterotopic aortic transplant if the sleeve technique is used. The approach we report in this study will help develop a better heterotopic aortic transplant model for basic and translational research on chronic rejection.…”
Section: Discussionmentioning
confidence: 81%
“…7 Chronic rejection models have been used widely to investigate the pathogenesis of chronic vascular rejection. [8][9][10][11][12][13] In conclusion, size discrepancy between donor and recipient aortas is not in obstacle in a mouse heterotopic aortic transplant if the sleeve technique is used. The approach we report in this study will help develop a better heterotopic aortic transplant model for basic and translational research on chronic rejection.…”
Section: Discussionmentioning
confidence: 81%
“…34 In relation to TA, elimination of recipient IL-6 slightly increases arteriosclerotic thickening in an aortic interposition model and systemic neutralization of this cytokine reduces arteriosclerotic thickening in a humanized model of vascular rejection. 35,36 Initially, after organ transplantation, the large majority of alloreactive T cells are activated toward allogeneic peptide-MHC presented by graft cells. 37 The mechanism by which IL-6 is immunostimulatory in our experiments is likely through its secretion by antigen presenting cells because we observe that IL-6 increases T cell proliferation and prevents T cell death in the spleen, which is a location where graft-derived antigen-presenting cells (but not vascular cells) affect T cell activation.…”
Section: Discussionmentioning
confidence: 99%
“…4 Furthermore, stimulation of macrophages with ApoE promotes their conversion from the proinflammatory M1 to the anti-inflammatory M2 phenotype 6 and suppresses the inflammatory response upon LPS stimulation. 7 Apolipoprotein E also inhibits platelet activation, aggregation, and regulates function of adaptive immunity including generation of cytotoxic T cells and production of immunoglobulin G. [8][9][10] Apolipoprotein E is composed of 2 distinct functional domains. The N-terminal domain that contains a receptorbinding region located between residues 133 and 149 and the C-terminal domain that includes a lipid-binding region.…”
mentioning
confidence: 99%