Abstract
Allogeneic hematopoietic stem cell transplantation (HSCT) is most commonly a treatment for inborn defects of hematopoiesis or acute leukemias. Widespread use of HSCT, a potentially curative therapy, is hampered by onset of graft-versus-host disease (GVHD), classified as either acute or chronic GVHD. While the pathology of acute GVHD is better understood, factors driving GVHD at the cellular and molecular level are less clear. Mast cells are an arm of the immune system that are known for atopic disease. However, studies have demonstrated that they can play important roles in tissue homeostasis and wound healing, and mast cell dysregulation can lead to fibrotic disease. Interestingly, in chronic GVHD, aberrant wound healing mechanisms lead to pathological fibrosis, but the cellular etiology driving this is not well-understood, although some studies have implicated mast cells. Given this novel role, we here review the literature for studies of mast cell involvement in the context of chronic GVHD. While there are few publications on this topic, the papers excellently characterized a niche for mast cells in chronic GVHD. These findings may be extended to other fibrosing diseases in order to better target mast cells or their mediators for treatment of fibrotic disease.
Highlights
Chronic graft versus host disease is a late complication that occurs in about 50 percent of patients that have undergone allogeneic hematopoietic stem cell transplant
In contrast to acute graft versus host disease, which is characterized by acute inflammation, massive cytokine production, and barrier dysfunction, Chronic graft versus host disease (cGVHD) appears much more autoimmune in its mechanisms of pathogenesis
Liver and skin fibrosis can both occur in cGVHD, but seem to do so by different mechanisms, with T follicular helper (Tfh) cells being more important for scleroderma, and Th17 cells being critical for development of liver fibrosis [24]
Summary
Chronic graft versus host disease (cGVHD) is a late complication that occurs in about 50 percent of patients that have undergone allogeneic hematopoietic stem cell transplant (allo-HSCT). In contrast to acute graft versus host disease (aGVHD), which is characterized by acute inflammation, massive cytokine production, and barrier dysfunction, cGVHD appears much more autoimmune in its mechanisms of pathogenesis. It is complex and poorly understood but is known to involve crosstalk and interactions between T-cells, B-cells, neutrophils, and tissue resident cells. CGVHD can affect any organ system, with key symptoms often related to increased collagen deposition These changes are often seen to be acellular, this can change depending on the disease presentation. While others have reviewed the field as it is currently known [1,8,9], there are still gaps in knowledge that need to be filled in order to better treat this progressive and debilitating disease
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