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SummaryHuman and murine stromal progenitor cells (SPCs) can suppress alloresponse in vitro, suggesting that SPCs may have clinical application toward prevention or treatment of graft‐versus‐host disease (GVHD). However, th eresults of in vivo studies have been conflicting. This study utilized an established murine model of acute GVHD to assess the ability of bone marrow derived murine SPCs (mSPCs) to prevent or treat GVHD. GVHD was established by transplantation of B6 bone marrow and spleen cells into lethally irradiated (900 cGy) B6 × BALB/c F1 recipients. mSPCs were administered using various dose and timing protocols designed to either prevent or treat GVHD. After transplantation, mice were monitored daily for weight and survival. Differences in symptom severity were compared using a clinical GVHD scoring system. All GVHD control mice died of lethal GVHD. All groups treated with mSPCs for the prevention of GVHD went on to develop clinical GVHD with no alteration of the disease course or severity compared to controls. Administration of mSPC after the development of GVHD failed to improve the disease course. We conclude that in this model, the ability of SPCs to suppress alloresponse in vitro does not correlate with in vivo prevention or treatment of acute GVHD.

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Most of our knowledge of mesenchymal stem cell (MSC) biology is derived from in vitro systems that are often highly contrived to favor culture expansion or specific differentiation events. However, any conclusions drawn from in vitro studies regarding MSC differentiation capacity, immune properties, or therapeutic potential must be validated by in vivo studies to ultimately be meaningful. At the present time, there are relatively few in vivo studies demonstrating differentiation and functional integration of MSCs into host tissues after transplantation. There is a need for in vivo model systems to assay MSC biology and to move potential therapeutic strategies forward. Here, we review prenatal model systems as potentially advantageous for the in vivo characterization of MSCs, and we critically review the results of in vivo studies of MSC transplantation in prenatal and postnatal model systems with an emphasis on proven engraftment and differentiation.

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MMR deficiency, potentially promoted by FOXO1 suppression, may explain the etiology for PTC development in some patients. FTC and FTA retain MMR activity and are likely caused by a different tumorigenic pathway.