Acute and chronic phagocyte determinants of cardiac allograft vasculopathy.

Published

Journal Article (Review)

Post-transplant immunosuppression has reduced the incidence of T cell-mediated acute rejection, yet long-term cardiac graft survival rates remain a challenge. An important determinant of chronic solid organ allograft complication is accelerated vascular disease of the transplanted graft. In the case of cardiac allograft vasculopathy (CAV), the precise cellular etiology remains inadequately understood; however, histologic evidence hints at the accumulation and activation of innate phagocytes as a causal contributing factor. This includes monocytes, macrophages, and immature dendritic cell subsets. In addition to crosstalk with adaptive T and B immune cells, myeloid phagocytes secrete paracrine signals that directly activate fibroblasts and vascular smooth muscle cells, both of which contribute to fibrous intimal thickening. Though maladaptive phagocyte functions may promote CAV, directed modulation of myeloid cell function, at the molecular level, holds promise for tolerance and prolonged cardiac graft function.

Full Text

Duke Authors

Cited Authors

  • Glinton, K; DeBerge, M; Yeap, X-Y; Zhang, J; Forbess, J; Luo, X; Thorp, EB

Published Date

  • November 2018

Published In

Volume / Issue

  • 40 / 6

Start / End Page

  • 593 - 603

PubMed ID

  • 30141073

Pubmed Central ID

  • 30141073

Electronic International Standard Serial Number (EISSN)

  • 1863-2300

International Standard Serial Number (ISSN)

  • 1863-2297

Digital Object Identifier (DOI)

  • 10.1007/s00281-018-0699-4

Language

  • eng