4.5 Review

Acute and chronic phagocyte determinants of cardiac allograft vasculopathy

Journal

SEMINARS IN IMMUNOPATHOLOGY
Volume 40, Issue 6, Pages 593-603

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00281-018-0699-4

Keywords

Transplant; Vasculopathy; Macrophage; Tolerance

Funding

  1. NHLBI [R01HL122309, R01HL139812-01]
  2. AHA post-doctoral award
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL139812, R01HL122309] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI114824] Funding Source: NIH RePORTER

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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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