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Detecting Rejection after Mouse Islet Transplantation Utilizing Islet Protein-Stimulated ELISPOT

Cell Transplantation. 2011;20 DOI 10.3727/096368910X539137

 

Journal Homepage

Journal Title: Cell Transplantation

ISSN: 0963-6897 (Print); 1555-3892 (Online)

Publisher: SAGE Publishing

LCC Subject Category: Medicine

Country of publisher: United States

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS


Christian Toso (Transplant Unit, Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland)

Rena Pawlick (Section of Hepatobiliary, Pancreatic and Transplant Surgery, University of Alberta, Edmonton, Canada)

Stéphanie Lacotte (Transplant Unit, Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland)

Ryan Edgar (Section of Hepatobiliary, Pancreatic and Transplant Surgery, University of Alberta, Edmonton, Canada)

Joy Davis (Section of Hepatobiliary, Pancreatic and Transplant Surgery, University of Alberta, Edmonton, Canada)

Michael McCall (Section of Hepatobiliary, Pancreatic and Transplant Surgery, University of Alberta, Edmonton, Canada)

Philippe Morel (Transplant Unit, Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland)

Gilles Mentha (Transplant Unit, Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland)

Thierry Berney (Transplant Unit, Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland)

A. M. James Shapiro (Section of Hepatobiliary, Pancreatic and Transplant Surgery, University of Alberta, Edmonton, Canada)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 15 weeks

 

Abstract | Full Text

Improved posttransplant monitoring and on-time detection of rejection could improve islet transplantation outcome. The present study explored the possibility of detecting harmful events after mouse islet transplantation measuring the immune responsiveness against islet extracts. Mouse islet transplantations were performed using various donor/recipient combinations, exploring autoimmune (NOD/SCID to NOD, n = 6) and alloimmune events (C57BL/6 to BALB/c, n = 20), a combination of both (C57BL/6 to NOD, n = 8), the absence of both (BALB/c to BALB/c, n = 21), or naive, nontransplanted control mice ( n = 14). The immune reactivity was measured by ELISPOT, looking at the ex vivo release of IFN-γ from splenocytes stimulated by islet donor extracts (sonicated islets). The immune reactivity was not altered in the syngeneic and autoimmune models, demonstrating similar levels as nontransplanted controls ( p = 0.46 and p = 0.6). Conversely, the occurrence of an allogeneic rejection alone or in combination to autoimmunity was associated to an increase in the level of immune reactivity ( p = 0.023 and p = 0.003 vs. respective controls). The observed increase was transient and lost in the postrejection period or after treatment with CTLA4-Ig. Overall, allogeneic rejection was associated to a transient increase in the reactivity of splenocytes against islet proteins. Such a strategy has the potential to improve islet graft monitoring in human and should be further explored.