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Immune-mediated vascular injury and dysfunction in transplant arteriosclerosis.

von Rossum A, Laher I, Choy JC - Front Immunol (2015)

Bottom Line: Solid organ transplantation is the only treatment for end-stage organ failure but this life-saving procedure is limited by immune-mediated rejection of most grafts.Blood vessels within transplanted organs are targeted by the immune system and the resultant vascular damage is a main contributor to acute and chronic graft failure.The vasculature is a unique tissue with specific immunological properties.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Biochemistry, Simon Fraser University , Burnaby, BC , Canada.

ABSTRACT
Solid organ transplantation is the only treatment for end-stage organ failure but this life-saving procedure is limited by immune-mediated rejection of most grafts. Blood vessels within transplanted organs are targeted by the immune system and the resultant vascular damage is a main contributor to acute and chronic graft failure. The vasculature is a unique tissue with specific immunological properties. This review discusses the interactions of the immune system with blood vessels in transplanted organs and how these interactions lead to the development of transplant arteriosclerosis, a leading cause of heart transplant failure.

No MeSH data available.


Related in: MedlinePlus

T cell-mediated effects on vasodilation and vasoconstriction in allograft arteries. (A) TNF and IL-17 are produced by T cells in allograft arteries. TNF acutely increases NO production from the endothelium by increasing eNOS activity through the up-regulation of tetrahydrobiopterin (BH4) synthesis. IL-17 increases NO production by increasing expression of eNOS. (B) IFNγ and TNF contribute to the vasoconstriction of allograft arteries by inhibiting the expression of eNOS, which reduces the levels of bioactive NO, as well as by increasing the production of the vasoconstrictive peptide ET-1.
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Figure 2: T cell-mediated effects on vasodilation and vasoconstriction in allograft arteries. (A) TNF and IL-17 are produced by T cells in allograft arteries. TNF acutely increases NO production from the endothelium by increasing eNOS activity through the up-regulation of tetrahydrobiopterin (BH4) synthesis. IL-17 increases NO production by increasing expression of eNOS. (B) IFNγ and TNF contribute to the vasoconstriction of allograft arteries by inhibiting the expression of eNOS, which reduces the levels of bioactive NO, as well as by increasing the production of the vasoconstrictive peptide ET-1.

Mentions: Besides intimal thickening, another change in allograft arteries that ultimately drives ischemic graft failure is vasomotor dysfunction. The vascular endothelium is essential for regulating arterial vasomotor function, acting on vascular smooth muscle cells to control the dilation and constriction of blood vessels (158–160). The balance between vasodilatory and vasoconstrictive factors, as well as the inherent myogenic properties of the smooth muscle, determines blood flow through arteries. This balance is disturbed in allograft arteries (Figure 2) (161–163).


Immune-mediated vascular injury and dysfunction in transplant arteriosclerosis.

von Rossum A, Laher I, Choy JC - Front Immunol (2015)

T cell-mediated effects on vasodilation and vasoconstriction in allograft arteries. (A) TNF and IL-17 are produced by T cells in allograft arteries. TNF acutely increases NO production from the endothelium by increasing eNOS activity through the up-regulation of tetrahydrobiopterin (BH4) synthesis. IL-17 increases NO production by increasing expression of eNOS. (B) IFNγ and TNF contribute to the vasoconstriction of allograft arteries by inhibiting the expression of eNOS, which reduces the levels of bioactive NO, as well as by increasing the production of the vasoconstrictive peptide ET-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4290675&req=5

Figure 2: T cell-mediated effects on vasodilation and vasoconstriction in allograft arteries. (A) TNF and IL-17 are produced by T cells in allograft arteries. TNF acutely increases NO production from the endothelium by increasing eNOS activity through the up-regulation of tetrahydrobiopterin (BH4) synthesis. IL-17 increases NO production by increasing expression of eNOS. (B) IFNγ and TNF contribute to the vasoconstriction of allograft arteries by inhibiting the expression of eNOS, which reduces the levels of bioactive NO, as well as by increasing the production of the vasoconstrictive peptide ET-1.
Mentions: Besides intimal thickening, another change in allograft arteries that ultimately drives ischemic graft failure is vasomotor dysfunction. The vascular endothelium is essential for regulating arterial vasomotor function, acting on vascular smooth muscle cells to control the dilation and constriction of blood vessels (158–160). The balance between vasodilatory and vasoconstrictive factors, as well as the inherent myogenic properties of the smooth muscle, determines blood flow through arteries. This balance is disturbed in allograft arteries (Figure 2) (161–163).

Bottom Line: Solid organ transplantation is the only treatment for end-stage organ failure but this life-saving procedure is limited by immune-mediated rejection of most grafts.Blood vessels within transplanted organs are targeted by the immune system and the resultant vascular damage is a main contributor to acute and chronic graft failure.The vasculature is a unique tissue with specific immunological properties.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Biochemistry, Simon Fraser University , Burnaby, BC , Canada.

ABSTRACT
Solid organ transplantation is the only treatment for end-stage organ failure but this life-saving procedure is limited by immune-mediated rejection of most grafts. Blood vessels within transplanted organs are targeted by the immune system and the resultant vascular damage is a main contributor to acute and chronic graft failure. The vasculature is a unique tissue with specific immunological properties. This review discusses the interactions of the immune system with blood vessels in transplanted organs and how these interactions lead to the development of transplant arteriosclerosis, a leading cause of heart transplant failure.

No MeSH data available.


Related in: MedlinePlus