Abstract
Kidney transplantation is the best treatment for end-stage renal disease, but its implementation is limited by organ shortage and immune rejection. Side effects of current immunosuppressive drugs, such as nephrotoxicity, opportunistic infection, and tumorigenic potential, influence long-term graft outcomes. In recent years, continued research and subsequent discoveries concerning the properties and potential utilization of mesenchymal stem cells (MSCs) have aroused considerable interest and expectations. Biological characteristics of MSCs, including multi-lineage differentiation, homing potential, paracrine effect and immunomodulation, have opened new horizons for applications in kidney transplantation. However, many studies have shown that the biological activity of MSCs depends on internal inflammatory conditions, and the safety and efficacy of the clinical application of MSCs remain controversial. This review summarizes the findings of a large number of studies and aims to provide an objective viewpoint based on a comprehensive analysis of the presently established benefits and obstacles of implementing MSC-based therapy in kidney transplantation, and to promote its clinical translation.
Highlights
The number of patients with chronic kidney disease and end-stage renal disease (ESRD) increases each year
Since its first long-term success in 1954, kidney transplantation has represented the best treatment for patients with ESRD
Immunosuppressive drugs taken by patients after transplantation heighten the risk of opportunistic infections and organ toxicity, which can affect the quality of life of patients as well as graft survival
Summary
The number of patients with chronic kidney disease and end-stage renal disease (ESRD) increases each year. We can speculate that the application of MSCs in kidney transplantation will reduce the amount of immunosuppressive drugs required, and enhance the renal function of patients and improve their longterm survival. MSC-mediated immunosuppression is elicited by interferon (IFN)-γ in the presence of other proinflammatory cytokines, tumor necrosis factor-α, interleukin (IL)1α, or IL-1β [9, 10] This activation step has been shown in vivo in a GVHD model, since recipients of IFN −/− T cells did not respond to MSC treatment and succumbed to GVHD [11]. MSCs exert immunosuppressive effects by secreting bioactive molecules and through cell-to-cell contact (Fig. 1) They can inhibit the activation of macrophages to release proinflammatory cytokines and promote antiinflammatory cytokine secretion. Other findings have shown that autologous MSCs injected together with a maintenance immunosuppressant resulted in
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