Suboptimal vitamin D levels are common in pediatric patients scheduled to receive HSCT and are associated with lower overall 1-year survival. Further study is warranted to delineate the mechanisms underlying the role of vitamin D in successful HSCT.
ly explained by donor hematopoietic cell gene expression. Gene expression of Ang2 and PlGF are lower in SR aGVHD, suggesting the plasma elevations in these factors might be predominantly host-derived. Ang2 likely reflects host endothelial tissue damage, while the PlGF response to aGVHD requires further investigation. The elevation in several damage-associated factors in the plasma and transcriptome in a healthy HCT recipient may reflect normal adaptation of donor cells to a new host. Mechanistic studies aimed at manipulating the dysregulated system of AF and downstream signaling pathways are indicated, with the goal of ameliorating severe aGVHD and facilitating tissue repair, without excess immunosuppression.
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