Abstract
Chronic rejection is the primary long-term complication in cardiac allografts, where it manifests as diffuse arteriosclerosis known as cardiac allograft vasculopathy (CAV). Although T, B and NK cells are implicated in its pathogenesis, the identity of the end-effectors that fuel CAV development is ill-defined. Because of their abundant presence in CAV lesions and their capacity to produce growth factors implicated in neointimal cell proliferation, macrophages are leading candidates to serve as these end-effectors.
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