Abstract
The state-of-the-art immunosuppression drugs do not ensure indefinite transplant survival, and most transplants are continuously lost to chronic rejection even years posttransplantation. This form of rejection is responsible for long-term failure of transplanted organs. The mechanisms involved in development of chronic rejection are not well-understood. One of the main features of chronic rejection is progressive luminal narrowing of graft vessels, which results in compromised blood flow, ischemia, cell death, and finally graft failure. All the existing immunosuppressive regimens are targeting acute rejection, and at present there is no available therapy for prevention of chronic rejection. Chronic rejection involves two major, but interrelated responses: The first is the host immune response against the transplant mediated primarily by alloreactive T and B cells, and the second is injury and repair of the graft (vasculopathy of graft vessels). Here we focus on recent advances in understanding the cellular and molecular aspects of chronic transplant vasculopathy and function of macrophages, topics pivotal for development of novel antichronic rejection therapies.
Highlights
There are three major types of allograft rejection: Hyperacute, acute, and chronic rejection.[1]
Marrow cells expressing smooth muscle specific α-actin. These data support the hypothesis of recipient origin of neointimal cells in native atherosclerosis, they do not prove that the same process occurs during chronic transplant rejection
This study showed that the loss of cells from the media of allograft vessels is the result of cytolytic cell-induced apoptosis, but not depopulation resulting from smooth muscle cells (SMCs) transmigration.[11]
Summary
There are three major types of allograft rejection: Hyperacute, acute, and chronic rejection.[1]. The assumption that SMCs originate exclusively from the donor has been recently challenged [Figure 4].[5,11,18] Using mouse vascular mechanical injury as a model of neointima formation in native atherosclerosis, Han et al.,[19] showed that neointimal cells can derive (at least partially) from the recipient bone a XX XXXXX b
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