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Accelerated acute rejection of the intestinal graft in CD28-deficient mice.

Artikel i vetenskaplig tidskrift
Författare G. Dindelegan
Mihai Oltean
Göran Kurlberg
Nils Y Lycke
Ola Nilsson
Michael Olausson
Publicerad i Transplantation proceedings
Volym 37
Nummer/häfte 1
Sidor 82-6
ISSN 0041-1345
Publiceringsår 2007
Publicerad vid Institutionen för biomedicin, avdelningen för patologi
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för kliniska vetenskaper
Sidor 82-6
Språk en
Länkar dx.doi.org/10.1016/j.transproceed.2...
Ämnesord Acute Disease, Animals, Antigens, CD28, genetics, Gene Deletion, Graft Rejection, genetics, immunology, pathology, Intestinal Mucosa, pathology, transplantation, Intestine, Small, parasitology, transplantation, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Microcirculation, immunology, pathology, Transplantation, Homologous, immunology, pathology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

OBJECTIVE: Multiple in vivo studies have shown that the pace and severity of graft rejection is little or not at all changed by deleting CD28 molecules in the recipient. These findings contrast with the effects of monoclonal antibody therapy aimed the same costimulatory target. The objective of the present study was to evaluate how the acute rejection process is affected in CD28-deficient mice using a fully allogeneic, highly immunologically reactive transplant model. METHODS: Heterotopic vascularized small bowel transplants were performed in 24 recipient mice divided into 4 groups: 2 wild-type and 2 knockout groups. Each group consisted of 5 to 7 animals in which BalbC mice were used as intestinal donors to either wild-type C57BL6 or C57BL6 background CD28-deficient recipient mice. Selected endpoints were 3 and 6 postoperative days (POD). Intestinal rejection was evaluated by mucosal laser Doppler flowmetry (expressed in perfusion units) and histology (expressed in rejection grades). RESULTS: Acute rejection occurred in both wild-type and CD28-deficient groups. At POD 3, no significant difference was noted between groups in terms of mucosal perfusion and histology. At POD 6, significant differences in graft mucosal perfusion and histology revealed a more aggressive rejection in the CD28-deficient group compared to the wild-type group. CONCLUSIONS: The present study showed that the severity of intestinal graft rejection responses was amplified by deleting CD28 molecules. Together with data from other studies, these results suggest a different pattern of distribution and/or activation of CD28/B7 receptors in various organs.

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