Acute and chronic phagocyte determinants of cardiac allograft vasculopathy

Kristofor Glinton, Matthew DeBerge, Xin Yi Yeap, Jenny Zhang, Joseph M Forbess, Xunrong Luo, Edward Benjamin Thorp*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)593-603
Number of pages11
JournalSeminars in Immunopathology
Issue number6
StatePublished - Nov 2018


  • Macrophage
  • Tolerance
  • Transplant
  • Vasculopathy

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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