Graft-versus-host disease represents the main side effect occurring after allogeneic stem cell transplantation hampering its potential curative effect. Acute GVHD still occurs in about 20-50% of the patients. The Success-rate of first-line treatment is still unchanged in recent years since it is still based on corticosteroids and is about 60%, with 40-50% of non-relapse mortality. Patients with chronic GVHD represent 30-60% of recipients, they usually undergo several lines of treatment and are affected by up to 40% non-relapse mortality.
First evidence pointed out the relevant effect of alloreactive Th1 cells and lack of Treg differentiation for acute and chronic GVHD pathogenesis, respectively. More recently several other actors have come into light such as Th17 and B cells, endothelial cells, innate-immunity mediators such as neutrophils, macrophages, innate lymphoid cells, gut microbiome, circulating microvesicles, etc. This new biological evidence are bringing renovated enthusiasm in the GVHD arena because they are translating into the development of new drugs with potential activity for the prevention or treatment of GVHD through several specific mechanisms such as inhibition of the JAK1/2 pathway, toll-like receptors, or IL-1 inhibitors, blockade of CSF-1R signaling, ROCK2 inhibitors, CTLA-4 blockade, IL-22 modulation, etc.
Hopefully, with the advent of these new drugs, the therapeutic scenario of GVHD prevention and treatment may finally improve, but up to date, the available armamentarium is still limited. In this Research Topic we welcome the submissions of Review, Mini Review, Perspective, Clinical Trial, and Original Research articles on the following, and related, subtopics:
- Prevention of acute and/or chronic GVHD: present strategies, limitations, and new immunologic mechanisms susceptible of modulation
- Pre-emption of chronic GVHD: early clinical signs and biological predictors
- Personalized therapy for chronic GVHD: new targeted therapies and biological insights
- Anti-fibrotic treatment for chronic GVHD
- Prognostic stratification of patients with acute and chronic GVHD and potential new front-line treatments
- Late acute-Overlap chronic GVHD-chronic GVHD: biological and clinical correlations
- Adoptive immunotherapy for treatment or prevention of GVHD
- Innate immunity: current evidence in the pathogenesis of GVHD and potential modulation strategies
- Endothelial damage in acute and chronic GVHD: current knowledge and potential targeted therapies
- Infectious complications after acute and/or chronic GVHD: current treatments and potential new targets
Graft-versus-host disease represents the main side effect occurring after allogeneic stem cell transplantation hampering its potential curative effect. Acute GVHD still occurs in about 20-50% of the patients. The Success-rate of first-line treatment is still unchanged in recent years since it is still based on corticosteroids and is about 60%, with 40-50% of non-relapse mortality. Patients with chronic GVHD represent 30-60% of recipients, they usually undergo several lines of treatment and are affected by up to 40% non-relapse mortality.
First evidence pointed out the relevant effect of alloreactive Th1 cells and lack of Treg differentiation for acute and chronic GVHD pathogenesis, respectively. More recently several other actors have come into light such as Th17 and B cells, endothelial cells, innate-immunity mediators such as neutrophils, macrophages, innate lymphoid cells, gut microbiome, circulating microvesicles, etc. This new biological evidence are bringing renovated enthusiasm in the GVHD arena because they are translating into the development of new drugs with potential activity for the prevention or treatment of GVHD through several specific mechanisms such as inhibition of the JAK1/2 pathway, toll-like receptors, or IL-1 inhibitors, blockade of CSF-1R signaling, ROCK2 inhibitors, CTLA-4 blockade, IL-22 modulation, etc.
Hopefully, with the advent of these new drugs, the therapeutic scenario of GVHD prevention and treatment may finally improve, but up to date, the available armamentarium is still limited. In this Research Topic we welcome the submissions of Review, Mini Review, Perspective, Clinical Trial, and Original Research articles on the following, and related, subtopics:
- Prevention of acute and/or chronic GVHD: present strategies, limitations, and new immunologic mechanisms susceptible of modulation
- Pre-emption of chronic GVHD: early clinical signs and biological predictors
- Personalized therapy for chronic GVHD: new targeted therapies and biological insights
- Anti-fibrotic treatment for chronic GVHD
- Prognostic stratification of patients with acute and chronic GVHD and potential new front-line treatments
- Late acute-Overlap chronic GVHD-chronic GVHD: biological and clinical correlations
- Adoptive immunotherapy for treatment or prevention of GVHD
- Innate immunity: current evidence in the pathogenesis of GVHD and potential modulation strategies
- Endothelial damage in acute and chronic GVHD: current knowledge and potential targeted therapies
- Infectious complications after acute and/or chronic GVHD: current treatments and potential new targets