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Abstract
Graft versus host disease (GVHD) is a common complication and the leading cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Pharmacological immunosuppression used in GVHD prophylaxis and treatment lacks specificity and can increase the likelihood of infection and relapse. Regulatory T lymphocytes (Tregs) play a vital role in restraining excessive immune responses and inducing peripheral immune tolerance. In particular, clinical trials have demonstrated that Tregs can prevent and treat GVHD, without increasing the risk of relapse and infection. Hence, adoptive transfer of Tregs to control GVHD using their immunosuppressive properties represents a promising therapeutic approach. To optimally apply Tregs for control of GVHD, a thorough understanding of their biology is necessary. In this review, we describe the biological characteristics of Tregs, including how the stability of FOXP3 expression can be maintained. We will also discuss the mechanisms underlying Tregs-mediated modulation of GVHD and approaches to effectively increase Tregs’ numbers. Finally, we will examine the developing trends in the use of Tregs for clinical therapy.
Highlights
Allogeneic hematopoietic stem-cell transplantation is a curative therapy for patients with many hematological malignancies; graft versus host disease (GVHD) is a major obstacle to the utility of allo-HSCT as it contributes to subsequent mortality and morbidity
Numerous animal studies have confirmed that Tregs have important roles in restraining excessive immune responses and can prevent Graft versus host disease (GVHD), without increasing the risk of relapse and infection
Upstream factors that regulate Tregs’ stability have not been clearly elucidated; strategies to maintain forkhead box P3 (FOXP3) stability warrant investigation to ensure that Tregs exert a suppressive function after adoptive transfer
Summary
Allogeneic hematopoietic stem-cell transplantation (allo-HSCT) is a curative therapy for patients with many hematological malignancies; graft versus host disease (GVHD) is a major obstacle to the utility of allo-HSCT as it contributes to subsequent mortality and morbidity. DCs can induce donor T cell tolerance by promoting the expansion and function of Tregs, protecting them from GVHD [60, 73]. This means that immunosuppressive Tregs controlling GVHD by inhibiting the initial activation of alloreactive T cells may compromise the GVL effect, thereby increasing the risk of relapse and infection.
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