Pathology of human intestinal transplantation

Rg, Lee; Nakamura, Kenjiro; Ac, Tsamandas; Abu‐Elmagd, Kareem; Furukawa, Hiroyuki; Wr, Hutson; Reyes, Jorgé; Tabasco-Minguillan, JS; Todo, S; Aj, Demetris

doi:10.1053/gast.1996.v110.pm8964408

Cited by 228 publications

(122 citation statements)

References 13 publications

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“…Compared with other solid organ allografts, a higher degree of immunosuppression is required to prevent SB allograft rejection (5,6), and rejection episodes occur despite aggressive treatment. It has been suggested that difficulties encountered in controlling SB allograft rejection are due to the unique environment of the mucosal immune system (7,8).…”

Section: S Mall Bowel (Sb)mentioning

confidence: 99%

Donor T Cell Activation Initiates Small Bowel Allograft Rejection Through an IFN-γ-Inducible Protein-10-Dependent Mechanism

Zhang¹,

Kaptanoğlu²,

Haddad

et al. 2002

The Journal of Immunology

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The poor success in controlling small bowel (SB) allograft rejection is partially attributed to the unique immune environment in the donor intestine. We hypothesized that Ag-induced activation of donor-derived T cells contributes to the initiation of SB allograft rejection. To address the role of donor T cell activation in SB transplantation, SB grafts from DO11.10 TCR transgenic mice (BALB/c, H-2Ld+) were transplanted into BALB/c (isografts), or single class I MHC-mismatched (Ld-deficient) BALB/c H-2dm2 (dm2, H-2Ld−) mutant mice (allografts). Graft survival was followed after injection of control or antigenic OVA323–339 peptide. Eighty percent of SB allografts developed severe rejection in mice treated with antigenic peptide, whereas <20% of allografts were rejected in mice treated with control peptide (p < 0.05). Isografts survived >30 days regardless of OVA323–339 administration. Activation of donor T cells increased intragraft expression of proinflammatory cytokine (IFN-γ) and CXC chemokine IFN-γ-inducible protein-10 mRNA and enhanced activation and accumulation of host NK and T cells in SB allografts. Treatment of mice with neutralizing anti-IFN-γ-inducible protein-10 mAb increased SB allograft survival in Ag-treated mice (67%; p < 0.05) and reduced accumulation of host T cells and NK cells in the lamina propria but not mesenteric lymph nodes. These results suggest that activation of donor T cells after SB allotransplantation induces production of a Th1-like profile of cytokines and CXC chemokines that enhance infiltration of host T cells and NK cells in SB allografts. Blocking this pathway may be of therapeutic value in controlling SB allograft rejection.

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Section: S Mall Bowel (Sb)mentioning

confidence: 99%

Donor T Cell Activation Initiates Small Bowel Allograft Rejection Through an IFN-γ-Inducible Protein-10-Dependent Mechanism

Zhang¹,

Kaptanoğlu²,

Haddad

et al. 2002

The Journal of Immunology

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“…At this point, the identification of acute rejection in bowel is accomplished by considering a constellation of findings, including clinical symptoms (e.g. increased ostomy output), endoscopy appearance and histopathological changes seen in the mucosal biopsy (9). The endoscopically obtained biopsy is typically considered the most accurate appraisal of the rejection process, but with the caveat that there is an adequate amount of tissue for assessment (10).…”

Section: Introductionmentioning

confidence: 99%

Mucosal Vascular Alterations in Isolated Small‐Bowel Allografts: Relationship to Humoral Sensitization

Ruiz

Garcia²,

Pappas

et al. 2003

American Journal of Transplantation

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Acute vascular rejection (AVR) in human small-bowel transplantation is an inadequately characterized entity whose frequency and severity is not well understood. As compared to severe AVR, changes identifying early, mild or evolving AVR are not known. We created a scoring system to evaluate subtle mucosal vascular changes and examined 188 biopsies from 21 patients obtained in the first 3 months post transplant. A majority of patients had a transient rise in vascular injury, often within 30 days of transplant. Small-vessel congestion and erythrocyte extravasation were the most common alterations. The vascular injury score was not related to acute cellular rejection, HLA type or HLA antigen disparities. However, the patients with the vascular changes had significantly higher peak panel reactive antibodies (PRA) and a higher incidence of positive T-cell and B-cell crossmatch. Finally, graft survival was significantly lower in the patients demonstrating the early vascular lesions. These data suggest that the vascular injury is partially associated with humoral presensitization of the recipient and may be a form of acute vascular rejection. Since these vascular changes are frequent, we advocate early post-transplant monitoring to identify and manage potentially high-risk patients.

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“…Rejection was diagnosed from histopathologic examination of endoscopically guided mucosal biopsies (19). Nutritional care consisted of gradual institution of enteric feeding and discontinuation of TPN.…”

Section: Posttransplant Managementmentioning

confidence: 99%

En Bloc Multivisceral and Kidney Transplantation in an HIV Patient: First Case Report

Koval

Khanna²,

Pallotta

et al. 2016

American Journal of Transplantation

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Pathology of human intestinal transplantation

Cited by 228 publications

References 13 publications

Donor T Cell Activation Initiates Small Bowel Allograft Rejection Through an IFN-γ-Inducible Protein-10-Dependent Mechanism

Donor T Cell Activation Initiates Small Bowel Allograft Rejection Through an IFN-γ-Inducible Protein-10-Dependent Mechanism

Mucosal Vascular Alterations in Isolated Small‐Bowel Allografts: Relationship to Humoral Sensitization

En Bloc Multivisceral and Kidney Transplantation in an HIV Patient: First Case Report

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