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

Land, W.; Agostinis, Patrizia; Gasser, Stephan; Garg, Abhishek D.; Linkermann, Andreas

doi:10.1111/ajt.14012

Cited by 66 publications

(56 citation statements)

References 159 publications

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“…Some researchers reported various instances where SNS model seemed to fail e.g. MHC‐mismatched kidney transplants from living donors performing better than MHC‐compatible kidneys from deceased donors or graft‐vs‐host disease being less severe in recipients that had gentle (rather than harsh) preconditioning treatments . Moreover, it was still not clear why adjuvants were mandatory to make bacterial or viral vaccines work effectively, despite latter's obvious microbial non‐self composition …”

Section: Historical Background: From Self/non‐self Model To Anti‐tumomentioning

confidence: 99%

“…The clinical reality is that, most conventional therapies (i.e. various chemotherapies, some forms of radiotherapy, and various targeted therapies) currently used for treating cancer patients, are quite likely to induce a mixture of TCD, inflammatory cell death, and ICD (Figure ) . Moreover, the older the cancer patient, the lesser is the probability of inducing apoptosis via anti‐cancer chemo‐/radiotherapy (vice versa for pediatric cancer patients) because with increasing age most cells in various adult organs become more refractory to apoptosis .…”

Section: Cancer Cell Death‐driven Immunity: Toward Efficient Clinicalmentioning

confidence: 99%

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Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses

Garg

Agostinis

2017

Immunological Reviews

339

275

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The immunogenicity of cancer cells is an emerging determinant of anti-cancer immunotherapy. Beyond developing immunostimulatory regimens like dendritic cell-based vaccines, immune-checkpoint blockers, and adoptive T-cell transfer, investigators are beginning to focus on the immunobiology of dying cancer cells and its relevance for the success of anticancer immunotherapies. It is currently accepted that cancer cells may die in response to anti-cancer therapies through regulated cell death programs, which may either repress or increase their immunogenic potential. In particular, the induction of immunogenic cancer cell death (ICD), which is hallmarked by the emission of damage-associated molecular patterns (DAMPs); molecules analogous to pathogen-associated molecular patterns (PAMPs) acting as danger signals/alarmins, is of great relevance in cancer therapy. These ICD-associated danger signals favor immunomodulatory responses that lead to tumor-associated antigens (TAAs)-directed T-cell immunity, which paves way for the removal of residual, treatment-resistant cancer cells. It is also emerging that cancer cells succumbing to ICD can orchestrate "altered-self mimicry" i.e. mimicry of pathogen defense responses, on the levels of nucleic acids and/or chemokines (resulting in type I interferon/IFN responses or pathogen response-like neutrophil activity). In this review, we exhaustively describe the main molecular, immunological, preclinical, and clinical aspects of immunosuppressive cell death or ICD (with respect to apoptosis, necrosis and necroptosis). We also provide an extensive historical background of these fields, with special attention to the self/non-self and danger models, which have shaped the field of cell death immunology.

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Section: Historical Background: From Self/non‐self Model To Anti‐tumomentioning

confidence: 99%

Section: Cancer Cell Death‐driven Immunity: Toward Efficient Clinicalmentioning

confidence: 99%

Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses

Garg

Agostinis

2017

Immunological Reviews

339

275

View full text Add to dashboard Cite

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“…Sepsis in general can result in multiple organ failure and death as a consequence of uncontrolled activation of the innate immune system with high circulating levels of pro-inflammatory cytokines such as interleukin 6 (IL-6), IL-8, IL-1β and tumor necrosis factor α (TNFα) (Nupponen et al, 2001; Santana et al, 2015). In addition to cytokines, adenosine triphosphate (ATP) comprises one of many host damage-associated-molecular-patterns (DAMPs) molecules released to the extracellular space during cell injury in response to invasive pathogens (Land et al, 2016; Ousingsawat et al, 2017). The level of extracellular ATP is sensed by P2Y and P2X receptors and serves a wide range of physiological functions including thrombocyte aggregation, taste, pain, and chemo-sensing (Burnstock, 2009).…”

Section: Introductionmentioning

confidence: 99%

P2X1, P2X4, and P2X7 Receptor Knock Out Mice Expose Differential Outcome of Sepsis Induced by α-Haemolysin Producing Escherichia coli

Greve

Skals

Fagerberg

et al. 2017

Front. Cell. Infect. Microbiol.

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α-haemolysin (HlyA)-producing Escherichia coli commonly inflict severe urinary tract infections, including pyelonephritis, which comprises substantial risk for sepsis. In vitro, the cytolytic effect of HlyA is mainly mediated by ATP release through the HlyA pore and subsequent P2X1/P2X7 receptor activation. This amplification of the lytic process is not unique to HlyA but is observed by many other pore-forming proteins including complement-induced haemolysis. Since free hemoglobin in the blood is known to be associated with a worse outcome in sepsis one could speculate that inhibition of P2X receptors would ameliorate the course of sepsis. Surprisingly, this study demonstrates that P2X1−/− and P2X4−/− mice are exceedingly sensitive to sepsis with uropathogenic E. coli. These mice have markedly lower survival, higher cytokine levels and activated intravascular coagulation. Quite the reverse is seen in P2X1−/− mice, which had markedly lower cytokine levels and less coagulation activation compared to controls after exposure to uropathogenic E. coli. The high cytokine levels in the P2X7−/− mouse are unexpected, since P2X7 is implicated in caspase-1-dependent IL-1β production. Here, we demonstrate that IL-1β production during sepsis with uropathogenic E. coli is mediated by caspase-8, since caspase-8 and RIPK3 double knock out mice show substantially lower cytokine during sepsis and increased survival after injection of TNFα. These data support that P2X7 and P2X4 receptor activation has a protective effect during severe E. coli infection.

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“…6 Thus, IRI might limit the effectiveness of immunosuppression in preventing CLAD. 6 Thus, IRI might limit the effectiveness of immunosuppression in preventing CLAD.…”

mentioning

confidence: 99%

A B cell–dependent pathway drives chronic lung allograft rejection after ischemia–reperfusion injury in mice

Watanabe

Martinu

Chruscinski

et al. 2019

American Journal of Transplantation

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Chronic lung allograft dysfunction (CLAD) limits long‐term survival after lung transplant (LT). Ischemia–reperfusion injury (IRI) promotes chronic rejection (CR) and CLAD, but the underlying mechanisms are not well understood. To examine mechanisms linking IRI to CR, a mouse orthotopic LT model using a minor alloantigen strain mismatch (C57BL/10 [B10, H‐2b] → C57BL/6 [B6, H‐2b]) and isograft controls (B6→B6) was used with antecedent minimal or prolonged graft storage. The latter resulted in IRI with subsequent airway and parenchymal fibrosis in prolonged storage allografts but not isografts. This pattern of CR after IRI was associated with the formation of B cell–rich tertiary lymphoid organs within the grafts and circulating autoantibodies. These processes were attenuated by B cell depletion, despite preservation of allograft T cell content. Our observations suggest that IRI may promote B cell recruitment that drives CR after LT. These observations have implications for the mechanisms leading to CLAD after LT.

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

Cited by 66 publications

References 159 publications

Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses

Cell death and immunity in cancer: From danger signals to mimicry of pathogen defense responses

P2X1, P2X4, and P2X7 Receptor Knock Out Mice Expose Differential Outcome of Sepsis Induced by α-Haemolysin Producing Escherichia coli

A B cell–dependent pathway drives chronic lung allograft rejection after ischemia–reperfusion injury in mice

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