Abstract
Viral pathogens have been implicated in the pathogenesis of GVHD. Skin rash due to GVHD resembles herpes simplex virus (HSV)-associated erythema multiforme (EM), in which HSV-infected CD34+ stem cells are stimulated to differentiate into antigen presenting CD1a+ DCs which reside in the skin epidermis and are known as Langerhans cells (LC). This differentiation involves increased E-cadherin expression. HSV-primed LCs present HSV protein to T-cells and lead to EM.
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