DAMP—Induced Allograft and Tumor Rejection: The Circle Is Closing

W. G. Land*, P. Agostinis, S. Gasser, A. D. Garg, A. Linkermann, Dietmar K. Abendroth, Dieter Adam, Hans Joachim Anders, Helmut P. Arbogast, Carla Baan, Seiamak Bahram, Jan Ulrich Becker, Joseph V. Bonventre, Jan Hinrich Bräsen, Lloyd G. Cantley, Anil Chandraker, Abdallah Daar, Ilse Daehn, Dushka Dragun, Jean Michel DubernardChristine S. Falk, Philippe Georgel, Douglas R. Green, Josep Grinyo, Mehmet Haberal, Hermann Haller, Philip F. Halloran, Jan Ole Heller, Alexandre Hertig, Luuk Hilbrands, Tobias B. Huber, Ottmar Janssen, Anthony M. Jevnikar, Allan D. Kirk, Richard N. Kitsis, Jerzy Kupiec-Weglinski, Ulrich Kunzendorf, Guido Kroemer, Christian Kurts, Daqing Ma, Jonathan Maltzman, Raimund Margreiter, Gilbert Massard, Konrad Messmer, Randall Morris, James Murphy, Björn Nashan, Andrew Oberst, Alberto Ortiz, Mike Overholtzer, Claudio Ponticelli, David M. Rothstein, Ana B. Sanz, Mario Schiffer, Bernd Schröppel, Kevin Schulte, S. Y. Seong, Jean Sibilia, Andrew M. Siedlecki, Hans Werner Sollinger, Terry B. Strom, Brent R. Stockwell, Attila J. Szabó, Wulf Tonnus, H. L. Trivedi, Stephan G. Tullius, Laurence A. Turka, Heth Turnquist, Peter Vandenabeele, Tom Vanden Berghe, Henning Walczak, Joel M. Weinberg, Philippe Wolf, Adrian Zierleyn

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

56 Scopus citations


The pathophysiological importance of the immunogenicity of damage-associated molecular patterns (DAMPs) has been pinpointed by their identification as triggers of allograft rejection following release from dying cells, such as after ischemia–reperfusion injury. In cancers, however, this strong trigger of a specific immune response gives rise to the success of cancer immunotherapy. Here, we review the recently literature on the pathophysiological importance of DAMP release and discuss the implications of these processes for allograft rejection and cancer immunotherapy, revealing a striking mechanistic overlap. We conclude that these two fields share a common mechanistic basis of regulated necrosis and inflammation, the molecular characterization of which may be helpful for both oncologists and the transplant community.

Original languageEnglish
Pages (from-to)3322-3337
Number of pages16
JournalAmerican Journal of Transplantation
Issue number12
StatePublished - 1 Dec 2016


  • basic (laboratory) research/science
  • cancer/malignancy/neoplasia
  • cell death
  • immune regulation
  • immunobiology
  • organ transplantation in general
  • rejection
  • rejection: antibody-mediated (ABMR)
  • translational research/science


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