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Updated: Aug 18, 2026

Induction of Intestinal Graft-versus-host Disease and Its Mini-endoscopic Assessment in Live Mice
Published on: February 11, 2019
[Graft-versus-host disease after organ transplantation: donor and host factors]
1Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan.
Graft-versus-host disease (GVHD) induced by organ transplantation is dependent on both the quality and quantity of lymphocytes included in the graft. Changes in the host immune function after surgery are also important factors in the development of this disease. Based on our experimental data, GVHD after organ transplantation is reviewed To test the reactivity of graft lymphocytes in in vivo, small bowel, liver pancreas/spleen, and heart/lung transplantations were performed using a rat in parent-to-F 1 hybrid combination. All of the lymphoid organ transplants induced lethal GVHD, while liver graft did not accelerated the disease after the transplantation procedure. Lymphocytes in liver grafts had a unique population and showed a low response against alloantigens in vivo. Surgical treatments also increased the susceptibility to GVHD, especially the ischemic-reperfusion procedure; Endogenous endotoxemia triggered by reperfusion promoted the development of lethal GVHD.
Graft-versus-host disease (GVHD) induced by organ transplantation is dependent on both the quality and quantity of lymphocytes included in the graft. Changes in the host immune function after surgery are also important factors in the development of this disease. Based on our experimental data, GVHD after organ transplantation is reviewed To test the reactivity of graft lymphocytes in in vivo, small bowel, liver pancreas/spleen, and heart/lung transplantations were performed using a rat in parent-to-F 1 hybrid combination. All of the lymphoid organ transplants induced lethal GVHD, while liver graft did not accelerated the disease after the transplantation procedure. Lymphocytes in liver grafts had a unique population and showed a low response against alloantigens in vivo. Surgical treatments also increased the susceptibility to GVHD, especially the ischemic-reperfusion procedure; Endogenous endotoxemia triggered by reperfusion promoted the development of lethal GVHD.
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