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

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 trigg...

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Bibliographic Details
Published in:American journal of transplantation 2016-12, Vol.16 (12), p.3322-3337
Main Authors: Land, W. G., Agostinis, P., Gasser, S., Garg, A. D., Linkermann, A.
Format: Article
Language:English
Subjects:
Allografts
Animals
basic (laboratory) research/science
Cancer
Cancer immunotherapy
cancer/malignancy/neoplasia
cell death
Graft rejection
Graft Rejection - immunology
Graft Rejection - pathology
Humans
immune regulation
Immune response
immunobiology
Immunogenicity
Immunotherapy
Inflammation - physiopathology
Ischemia
Necrosis
Neoplasms - immunology
Neoplasms - pathology
organ transplantation in general
rejection
rejection: antibody‐mediated (ABMR)
Reperfusion
Reperfusion Injury - immunology
Reperfusion Injury - pathology
translational research/science
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Summary: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. Damage‐associated molecular patterns are released from both allografts and cancer cells, thereby stimulating immune cells in an astonishingly similar fashion.
ISSN:1600-6135
1600-6143
DOI:10.1111/ajt.14012