**4. Cases at Kyoto University Hospital**

*Organ Donation and Transplantation*

FasL and Fas, suggesting that the apoptosis relates to the FasL-Fas interactive reaction (**Figure 2**, lower panels). This result was first reported in our previous study [18].

*FasL immunostaining of the intestinal allograft. FasL-positive lymphocytes in the lamina propria (upper left, 200×) and Peyer's patch (upper right, 400×) are shown. FasL-stained apoptotic bodies (lower left, 400×). Apoptotic TCRV*α*24 stained cells (lower right, 400×). TCRV*α*24 and FasL were visualized with DAB* 

Endoscopically, elevation of the small intestinal mucosa may be recognized and biopsied when clinical rejection is suspected. Since this elevation is observed in patients who are not receiving oral nutrition, the change may not be the result of irritation from the lumen of the small intestine and more likely due to the reaction of the Peyer's patches (PPs) to a load of patient cells on the graft mucosal immune system. In our cases, the biopsied Peyer's patches were injured at the onset of ACR (**Figures 3A** and **B**). Therefore, PP is one of the targets of ACR or other types of rejection (**Figure 3C**). Notably, B cells increased in number in the disintegrated PPs (**Figure 3**). As described later, IL-5 was increased in the intestinal allograft [17],

*Histology of a PP in an intestinal allograft. (A, B) A hyperplastic Peyer's patch stained with CD79a antibody before ACR (A) and at the onset of ACR (B). (C) CD8 staining of PP after 42 h at the onset of rejection. Many* 

*CD8+ CTLs infiltrate in PP. CD79 and CD8 were visualized by DAB. The photo magnitude is 100×.*

**3. Endoscopic examination and Peyer's patch response**

which may promote the transient B cell growth in PP.

**92**

**Figure 3.**

**Figure 2.**

*(3,3'-diaminobenzidine).*

Here we review cases of SBT at Kyoto University Hospital [17, 18, 21, 22]. SBT was performed owing to intestinal malrotation and Hirschsprung's disease-related effects (**Figure 4**).

Jejunal or ileal grafts were monitored histologically. When fever, increased intestinal juice, abdominal pain, or C-reactive protein (CRP) elevation in peripheral blood (>0.5 mg/10−1 L) was observed, an endoscopic examination was performed. In particular, for the first 1 to 2 weeks after surgery, the examination was performed every other day, and a histological examination was also performed. Once the condition of the patient became stable, a histological examination was performed approximately once a week, and the state of the intestinal graft was monitored continuously for up to 2 months in the hospital. The patient received immunosuppressive therapy in combination with tacrolimus (trough concentration: 20 ng/mL) and methylprednisolone (30 mg/kg/day, 1 to 3 times). In the biopsy examination, diagnosis by hematoxylin and eosin staining and findings specific to rejection within 6 h were confirmed by immunostaining of frozen sections. For histological diagnosis, we stained the apoptosis-related proteins such as FasL and surface antigens of B cells, T cells, and NK cells in each case. Steroid pulse therapy was conducted following
