Macrophages in chronic rejection (IMAGE)
Caption
Organ harvest from a donor and subsequent restoration of blood flow after transplantation cause ischemia–reperfusion injury (IRI) of the transplant. First, donor macrophages residing in the transplanted organ are activated by cellular damage and the release of reactive oxygen species (ROS), polarizing into proinflammatory macrophages. Such macrophages produce inflammatory factors, such as IL-6, TNF-α, and MCP-1/CCL2, which promote further tissue damage, exacerbate inflammation, and recruit recipient macrophages and other immune cells to the graft, thereby potentiating the rejection response. Importantly, M1-like macrophages also promote vessel occlusion (neointima formation) through TNF-α-dependent induction of smooth muscle cell (SMC) proliferation and migration. Over time, these M1-like macrophages transition to an anti-inflammatory M2-like phenotype, which promotes tissue repair, fibrosis, and remodeling of the transplant tissue. In transplanted hearts, these M2-like macrophages produce fibrogenic factors, such as TGF-β, which facilitate the transformation of cardiac fibroblasts into myofibroblasts that induce collagen synthesis, extracellular matrix formation, and fibrosis, ultimately contributing to chronic graft rejection.
Credit
Professor Malgorzata Kloc from Houston Methodist Hospital, USA Image source link: https://link.springer.com/article/10.1007/s44466-026-00046-0
Usage Restrictions
Credit must be given to the creator. Only noncommercial uses of the work are permitted. No derivatives or adaptations of the work are permitted.
License
CC BY-NC-ND