Abstract
Despite decades of experience with hematopoietic stem cell transplantation, we are still faced with the delicate equipoise of achieving stable ocular health post-transplantation. This is because ocular graft-versus-host disease (oGvHD) following hematopoietic stem cell transplantation frequently occurs (≥50%) among transplant patients. To date, our understanding of the pathophysiology of oGvHD especially the involvement of the meibomian gland is still limited as a result of a lack of suitable preclinical models among other. Herein, the current state of the etiology and, pathophysiology of oGvHD based on existing pre-clinical models are reviewed. The need for additional pre-clinical models and knowledge about the involvement of the meibomian glands in oGvHD are emphasized.
Highlights
Allogeneic hematopoietic stem cell transplantation from human leukocyte antigen (HLA) matched donors is widely used as treatment for a myriad of hematological diseases, autoimmune diseases and inherited metabolic disorders [1,2,3]
graft-versus-host disease (GvHD) involves an exaggerated donor-derived lymphocytic reaction to host antigens following aHSTC. These host antigens are called minor histocompatibility antigens (MiHA) and are not included in routine HLA typing as part of the attempts to optimize the outcome of Allogeneic hematopoietic stem cell transplantation (aHSCT) [4]
In this review we summarize and present information on the current of state of ocular graft-versus-host disease (oGvHD) with emphasis on pre-clinical models
Summary
Allogeneic hematopoietic stem cell transplantation (aHSCT) from human leukocyte antigen (HLA) matched donors (related or unrelated) is widely used as treatment for a myriad of hematological diseases, autoimmune diseases and inherited metabolic disorders [1,2,3]. The most common form is chronic oGvHD which is accompanied by symptoms such as ocular discomfort, irritation, photophobia, redness, itchiness, foreign body sensation, burning, watery eyes and blurred vision [3,8] These hallmarks of oGvHD makes the condition mimic other immune conditions such as Sjogren’s or non-Sjogren-associated dry eye, making it clinically challenging to establish definitive diagnosis for oGvHD. There is the suggestion that it comprises at least three main biological processes; lacrimal gland dysfunction, corneo-conjunctival inflammation, and meibomian gland dysfunction (MGD) [7,11] The former two processes have been well studied but little information is known about the latter, that is the involvement of the meibomian glands and their dysfunction thereof in the development of oGvHD [7,13,14,15]. We further discuss the need for suitable animal models that better mimic the human oGvHD condition and suggest study strategies that can enhance our understanding of the involvement of the meibomian glands in oGvHD [7]
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