Unknown

Dataset Information

0

Interleukin (IL)-1 promotes allogeneic T cell intimal infiltration and IL-17 production in a model of human artery rejection.


ABSTRACT: Interleukin (IL) 1alpha produced by human endothelial cells (ECs), in response to tumor necrosis factor (TNF) or to co-culture with allogeneic T cells in a TNF-dependent manner, can augment the release of cytokines from alloreactive memory T cells in vitro. In a human-mouse chimeric model of artery allograft rejection, ECs lining the transplanted human arteries express IL-1alpha, and blocking IL-1 reduces the extent of human T cell infiltration into the artery intima and selectively inhibits IL-17 production by infiltrating T cells. In human skin grafts implanted on immunodeficient mice, administration of IL-17 is sufficient to induce mild inflammation. In cultured cells, IL-17 acts preferentially on vascular smooth muscle cells rather than ECs to enhance production of proinflammatory mediators, including IL-6, CXCL8, and CCL20. Neutralization of IL-17 does not reduce T cell infiltration into allogeneic human artery grafts, but markedly reduces IL-6, CXCL8, and CCL20 expression and selectively inhibits CCR6(+) T cell accumulation in rejecting arteries. We conclude that graft-derived IL-1 can promote T cell intimal recruitment and IL-17 production during human artery allograft rejection, and suggest that targeting IL-1 in the perioperative transplant period may modulate host alloreactivity.

SUBMITTER: Rao DA 

PROVIDER: S-EPMC2605225 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature

altmetric image

Publications

Interleukin (IL)-1 promotes allogeneic T cell intimal infiltration and IL-17 production in a model of human artery rejection.

Rao Deepak A DA   Eid Raymond E RE   Qin Lingfeng L   Yi Tai T   Kirkiles-Smith Nancy C NC   Tellides George G   Pober Jordan S JS  

The Journal of experimental medicine 20081215 13


Interleukin (IL) 1alpha produced by human endothelial cells (ECs), in response to tumor necrosis factor (TNF) or to co-culture with allogeneic T cells in a TNF-dependent manner, can augment the release of cytokines from alloreactive memory T cells in vitro. In a human-mouse chimeric model of artery allograft rejection, ECs lining the transplanted human arteries express IL-1alpha, and blocking IL-1 reduces the extent of human T cell infiltration into the artery intima and selectively inhibits IL-  ...[more]

Similar Datasets

| S-EPMC6044435 | biostudies-literature
| S-EPMC3757499 | biostudies-literature
| S-EPMC3491488 | biostudies-literature
| S-EPMC3988482 | biostudies-literature
| S-EPMC3123037 | biostudies-literature
| S-EPMC5098156 | biostudies-literature
| S-EPMC5314955 | biostudies-literature
| S-EPMC2779161 | biostudies-literature
| S-EPMC2928960 | biostudies-literature
| S-EPMC10866453 | biostudies-literature