| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
*
Immunobiology Research Center, Department of Surgery, Beth Israel Deaconess Medical Center, Boston, MA 02215; and
Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02215
Hamster hearts transplanted into transiently complement-depleted and continuously cyclosporin A (CyA)-immunosuppressed rats survive long-term despite deposition of anti-donor IgM Abs and complement on the graft vascular endothelium. This phenomenon is referred to as "accommodation." The hypothesis tested here is that accommodated xenografts are resistant to IgM Abs and complement that could result in rejection of naive xenografts. After first hamster hearts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days, a time when the anti-donor IgM Ab level was maximal and complement activity had returned to approximately 50% of pretreatment levels, naive hamster hearts or hamster hearts that had been accommodating in another rat for 14 days were transplanted into those rats carrying the surviving first graft. The naive hearts were all hyperacutely rejected. In contrast, a majority of regrafted accommodating hearts survived long-term. There was widespread Ab and activated complement deposition on the vascular endothelium of accommodating first hearts, second accommodating hearts, and rejected second naive hearts. However, only the rejected naive hearts showed extensive endothelial cell damage, myocardial necrosis, fibrin deposition, and other signs of inflammation. Accommodating first and second hearts but not rejected second naive hearts expressed high levels of the protective genes A20, heme oxygenase-1 (HO-1), bcl-2, and bcl-xL. These data demonstrate that accommodated xenografts become resistant to effects of anti-donor IgM Abs and complement that normally mediate rejection of xenografts. We hypothesize that this resistance involves expression by accommodated xenografts of protective genes.
This article has been cited by other articles:
|
|
 |
|
  P. T. Jindra, A. Hsueh, L. Hong, D. Gjertson, X.-D. Shen, F. Gao, J. Dang, P. S. Mischel, W. M. Baldwin III, M. C. Fishbein, et al. Anti-MHC Class I Antibody Activation of Proliferation and Survival Signaling in Murine Cardiac Allografts J. Immunol., February 15, 2008; 180(4): 2214 - 2224. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. C. Kirkiles-Smith, K. Mahboubi, J. Plescia, J. M. McNiff, J. Karras, J. S. Schechner, D. C. Altieri, and J. S. Pober IL-11 Protects Human Microvascular Endothelium from Alloinjury In Vivo by Induction of Survivin Expression J. Immunol., February 1, 2004; 172(3): 1391 - 1396. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Pileggi, R. D. Molano, T. Berney, P. Cattan, C. Vizzardelli, R. Oliver, C. Fraker, C. Ricordi, R. L. Pastori, F. H. Bach, et al. Heme Oxygenase-1 Induction in Islet Cells Results in Protection From Apoptosis and Improved In Vivo Function After Transplantation Diabetes, September 1, 2001; 50(9): 1983 - 1991. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Sato, J. Balla, L. Otterbein, R. N. Smith, S. Brouard, Y. Lin, E. Csizmadia, J. Sevigny, S. C. Robson, G. Vercellotti, et al. Carbon Monoxide Generated by Heme Oxygenase-1 Suppresses the Rejection of Mouse-to-Rat Cardiac Transplants J. Immunol., March 15, 2001; 166(6): 4185 - 4194. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Lin, M. P. Soares, K. Sato, E. Csizmadia, S. C. Robson, N. Smith, and F. H. Bach Long-Term Survival of Hamster Hearts in Presensitized Rats J. Immunol., May 1, 2000; 164(9): 4883 - 4892. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
