About this Research Topic
Allogeneic hematopoietic stem cell transplantation (aHSCT) represents a potential therapy for patients with a variety of life-threatening conditions, including hematopoietic malignancies, immune deficiency syndrome, and genetic disorders. However, the development of graft-versus-host disease (GVHD) remains a major obstacle to long-term transplant success following aHSCT. It is associated with significant morbidity and mortality and is the leading cause of non-relapse mortality.
GVHD occurs when donor T cells are primed by recipient antigens subsequently eliciting an inflammatory response against the host. Clinically, two types of GVHD are distinguishable: an acute form (aGVHD), with a typical early onset btw. 3-12 weeks and a chronic form (cGVHD), which is usually diagnosed less than 6 months post HSCT. aGVHDoccurs in 30-50% of aHSCTs and is a multi-organ disorder resulting from inflammatory cytokines and donor T cells which primarily damage skin, liver, gastrointestinal tract, and eye. cGVHD, with a prevalence of 30-70% of aHSCTs, is induced by T and B cells resulting in a heterogeneous immunological complication affecting virtually every organ.
Traditionally, broad immune-suppressive drugs (with considerable toxicities) including calcineurin inhibitors (CNI) (cyclosporin or tacrolimus), together with methotrexate or mycophenolate mofetil (MMF), and mTOR inhibitors (Sirolimus/Rapamycin) are used as GVHD prophylaxis. But despite first success reports, significant GVHD still occurs with these drugs. Other prophylaxis strategies like pre-transplant anti-thymocyte globulin (ATG) are effective in reducing severe GVHD but have no survival benefits and steroids have serious side effects.
One of the most critical challenges in aHSCT is the development of less toxic and more targeted therapies that maintain the GVL effect but suppress GVHD while facilitating enhanced immune reconstitution relative to existing strategies. Recently, several prophylaxis strategies for GVHD have been developed and others are currently in development, including, for example, post-transplant Cyclophosphamide (PTCy) and cytokines, which seem to be very promising.
In this Research Topic, we welcome the submission of Original Research, Reviews, Mini-Reviews, and Clinical Trials article on “Novel and improved methods for the prevention and amelioration/treatment of GVHD” that address, but are not limited to, the following sub-topics:
• Regulatory T cells (Treg)
• Post-transplant Cyclophosphamide (PTCy)
• NK cells
• Cytokines (e.g. IL-2)
• Myeloid-derived suppressor cells (MDSCs)
• Mesenchymal stem cells
• Tolerogenic DCs
• Extracorporeal photopheresis
• Small molecule inhibitors
• Antibodies and biologicals
• Biomarker profile for the risk stratification and treatment of GVHD
GVHD occurs when donor T cells are primed by recipient antigens subsequently eliciting an inflammatory response against the host. Clinically, two types of GVHD are distinguishable: an acute form (aGVHD), with a typical early onset btw. 3-12 weeks and a chronic form (cGVHD), which is usually diagnosed less than 6 months post HSCT. aGVHDoccurs in 30-50% of aHSCTs and is a multi-organ disorder resulting from inflammatory cytokines and donor T cells which primarily damage skin, liver, gastrointestinal tract, and eye. cGVHD, with a prevalence of 30-70% of aHSCTs, is induced by T and B cells resulting in a heterogeneous immunological complication affecting virtually every organ.
Traditionally, broad immune-suppressive drugs (with considerable toxicities) including calcineurin inhibitors (CNI) (cyclosporin or tacrolimus), together with methotrexate or mycophenolate mofetil (MMF), and mTOR inhibitors (Sirolimus/Rapamycin) are used as GVHD prophylaxis. But despite first success reports, significant GVHD still occurs with these drugs. Other prophylaxis strategies like pre-transplant anti-thymocyte globulin (ATG) are effective in reducing severe GVHD but have no survival benefits and steroids have serious side effects.
One of the most critical challenges in aHSCT is the development of less toxic and more targeted therapies that maintain the GVL effect but suppress GVHD while facilitating enhanced immune reconstitution relative to existing strategies. Recently, several prophylaxis strategies for GVHD have been developed and others are currently in development, including, for example, post-transplant Cyclophosphamide (PTCy) and cytokines, which seem to be very promising.
In this Research Topic, we welcome the submission of Original Research, Reviews, Mini-Reviews, and Clinical Trials article on “Novel and improved methods for the prevention and amelioration/treatment of GVHD” that address, but are not limited to, the following sub-topics:
• Regulatory T cells (Treg)
• Post-transplant Cyclophosphamide (PTCy)
• NK cells
• Cytokines (e.g. IL-2)
• Myeloid-derived suppressor cells (MDSCs)
• Mesenchymal stem cells
• Tolerogenic DCs
• Extracorporeal photopheresis
• Small molecule inhibitors
• Antibodies and biologicals
• Biomarker profile for the risk stratification and treatment of GVHD
Keywords: Graft-Versus-Host Disease, prevention, treatment, Treg, Cytokines, Small molecule inhibitors, Biomarker profile, NK cells, Myeloid derived suppressor cells
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