A subpopulation of parental to hybrid VBMT recipients developed characteristic clinical and histopathologic manifestations of GVHD. These changes are similar to those seen in human GVHD secondary to bone marrow transplantation. Human GVHD also manifests itself in an acute and chronic manner. Only a minority (30% to 40%) of animals developed lethal GVHD in our model. Those animals developing GVHD had a significantly (P < .0001) higher expression of TGF-beta in situ compared to the tolerant subpopulation. The differential expression of TGF-beta may represent an important mechanism of immune dysregulation associated with GVHD in CTA recipients.
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