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 journalArticle

Abstract

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)
JournalSeminars in Immunopathology
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Phagocytes
Allografts
Myeloid Cells
Transplants
Tunica Intima
Graft Survival
Vascular Diseases
Vascular Smooth Muscle
Immunosuppression
Dendritic Cells
Smooth Muscle Myocytes
Monocytes
Fibroblasts
Macrophages
T-Lymphocytes
Incidence

Keywords

  • Macrophage
  • Tolerance
  • Transplant
  • Vasculopathy

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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title = "Acute and chronic phagocyte determinants of cardiac allograft vasculopathy",
abstract = "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.",
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author = "Kristofor Glinton and Matthew DeBerge and Yeap, {Xin Yi} and Jenny Zhang and Forbess, {Joseph M} and Xunrong Luo and Thorp, {Edward Benjamin}",
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Acute and chronic phagocyte determinants of cardiac allograft vasculopathy. / Glinton, Kristofor; DeBerge, Matthew; Yeap, Xin Yi; Zhang, Jenny; Forbess, Joseph M; Luo, Xunrong; Thorp, Edward Benjamin.

In: Seminars in Immunopathology, 01.01.2018.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Acute and chronic phagocyte determinants of cardiac allograft vasculopathy

AU - Glinton, Kristofor

AU - DeBerge, Matthew

AU - Yeap, Xin Yi

AU - Zhang, Jenny

AU - Forbess, Joseph M

AU - Luo, Xunrong

AU - Thorp, Edward Benjamin

PY - 2018/1/1

Y1 - 2018/1/1

N2 - 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.

AB - 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.

KW - Macrophage

KW - Tolerance

KW - Transplant

KW - Vasculopathy

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